Dorsal Aortic Blood Pressure Research Articles

Seawater acclimation affects cardiac output and adrenergic control of blood pressure in rainbow trout (Oncorhynchus mykiss)-implications for salinity variations now and in the future.

Greater salinity variations resulting from ongoing climate change requires consideration in conservation management as this may impact on the performance of aquatic organisms. Euryhaline fish exhibit osmoregulatory flexibility and can exploit a wide range of salinities. In seawater (SW), they drink and absorb water in the intestine, which is associated with increased gastrointestinal blood flow. Yet, detailed information on other cardiovascular changes and their control across salinities is scant. Such knowledge is fundamental to understand how fish are affected during migrations between environments with different salinities, as well as by increased future salinity variability. We used rainbow trout (Oncorhynchus mykiss) as a euryhaline model species and determined dorsal aortic blood pressure, cardiac output and systemic vascular resistance in vivo after chronic freshwater-or SW-acclimation. We also assessed α-adrenergic control of blood pressure using pharmacological tools. Dorsal aortic blood pressure and systemic vascular resistance were reduced, whereas cardiac output increased in SW. α-Adrenergic stimulation with phenylephrine caused similar dose-dependent increases in resistance and pressure across salinities, indicating unaltered α-adrenoceptor sensitivity. α-Adrenergic blockade with prazosin decreased resistance and pressure across salinities, but the absolute reduction in resistance was smaller in SW. Yet, both pressure and resistance after prazosin remained consistently lower in SW. This shows that SW-acclimation lowers systemic resistance through reduced vascular α-adrenergic tone, along with other unknown vasodilating factors. The marked changes in adrenergic regulation of the vasculature across salinities discovered here may have implications for cardiovascular and aerobic performance of fishes, with possible impacts on fitness-related traits like digestion and exercise capacity. Moreover, the evolution of more complex circulatory control systems in teleost fishes compared with elasmobranchs and cyclostomes may have been an important factor in the evolution of euryhalinity, and may provide euryhaline teleosts with competitive advantages in more variable salinity environments of the future.

Effects of peripherally administered urotensin II and arginine vasotocin on the QT interval of the electrocardiogram in trout

The QT interval of the electrocardiogram (ECG) is a measure of the duration of the ventricular depolarization and repolarization. In fish as in human, the QT interval is positively correlated with the RR interval of the ECG, a measure of the cardiac cycle length. Urotensin II (UII) is a neuropeptide that has been highly conserved from fish to human, and UII and its receptor (UT) are expressed in cardiovascular tissues including the heart. Although UII exerts potent cardiovascular actions, its possible effects on the QT interval have never been investigated. The goal of the present study was to provide insight into the potential effect of UII on the QT interval in an established in vivo trout model. To this end, the effects of UII on dorsal aortic blood pressure (PDA), RR, QT intervals and corrected QT (QTc) for RR interval, were investigated after intra-arterial (IA) injection of 5, 50 and 100pmol UII. The effects of UII were compared to those of two structurally UII-related peptides (URPs), URP1 and URP2, and to those of arginine vasotocin (AVT), homolog of the mammalian arginine vasopressin. IA injection of vehicle or 5pmol UII had no effect on the various parameters. At the 50-pmol dose, UII evoked its usual increase in PDA with a peak value observed 15min after the injection (+22% from baseline, P<0.001). This hypertensive effect of UII was accompanied by a significant increase in the RR interval (+18%, P<0.001), i.e. a bradycardia, and these effects remained constant until the end of the recording. The highest dose of UII evoked similar hypertensive and bradycardic effects. Of interest, the QT interval did not change during the bradycardic action of UII (50 and 100pmol) but the QTc interval significantly decreased. In trout pre-treated with urantide, a peptidic antagonist of UT, the hypertensive and bradycardic actions of 50pmol UII were reduced 3-fold and no change occurred in the QT and QTc intervals. In trout pre-treated with blockers of the autonomic nervous system, the hypertensive effect of UII was maintained but no change appeared in RR, QT and QTc intervals. IA injections of 50pmol URPs were without action on the preceding parameters. IA administration of 50pmol AVT provoked quite similar increase in PDA, and elevation of the RR interval to those evoked by IA injection of UII but, in contrast to UII, AVT injection induced a highly significant and sustained prolongation of the QT interval compared to baseline (+7%, P<0.001) without change in QTc. Our results are indicative of a lack of QT interval change during UII-evoked bradycardia but not after AVT-induced bradycardia and suggest for the first time that some compensatory mechanism specific for the UII peptide is working to stabilize the QT interval. Further research is needed to elucidate the mechanism involved in this action of UII. The potential for UII to prevent detrimental prolongation of cardiac ventricular repolarization might be questioned.

Divergent cardio-ventilatory and locomotor effects of centrally and peripherally administered urotensin II and urotensin II-related peptides in trout.

The urotensin II (UII) gene family consists of four paralogous genes called UII, UII-related peptide (URP), URP1 and URP2. UII and URP peptides exhibit the same cyclic hexapeptide core sequence (CFWKYC) while the N- and C-terminal regions are variable. UII, URP1, and URP2 mRNAs are differentially expressed within the central nervous system of teleost fishes, suggesting that they may exert distinct functions. Although the cardiovascular, ventilatory and locomotor effects of UII have been described in teleosts, much less is known regarding the physiological actions of URPs. The goal of the present study was to compare the central and peripheral actions of picomolar doses (5–500 pmol) of trout UII, URP1, and URP2 on cardio-ventilatory variables and locomotor activity in the unanesthetized trout. Compared to vehicle, intracerebroventricular injection of UII, URP1 and URP2 evoked a gradual increase in total ventilation (VTOT) reaching statistical significance for doses of 50 and 500 pmol of UII and URP1 but for only 500 pmol of URP2. In addition, UII, URP1 and URP2 provoked an elevation of dorsal aortic blood pressure (PDA) accompanied with tachycardia. All peptides caused an increase in locomotor activity (ACT), at a threshold dose of 5 pmol for UII and URP1, and 50 pmol for URP2. After intra-arterial (IA) injection, and in contrast to their central effects, only the highest dose of UII and URP1 significantly elevated VTOT and ACT. UII produced a dose-dependent hypertensive effect with concomitant bradycardia while URP1 increased PDA and heart rate after injection of only the highest dose of peptide. URP2 did not evoke any cardio-ventilatory or locomotor effect after IA injection. Collectively, these findings support the hypothesis that endogenous UII, URP1 and URP2 in the trout brain may act as neurotransmitters and/or neuromodulators acting synergistically or differentially to control the cardio-respiratory and locomotor systems. In the periphery, the only physiological actions of these peptides might be those related to the well-known cardiovascular regulatory actions of UII. It remains to determine whether the observed divergent physiological effects of UII and URPs are due to differential interaction with the UT receptor or binding to distinct UT subtypes.

Effects of intracerebroventricular administered fluoxetine on cardio-ventilatory functions in rainbow trout (Oncorhynchus mykiss)

Fluoxetine (FLX) is a selective serotonin (5-HT) reuptake inhibitor present in the aquatic environment which is known to bioconcentrate in the brains of exposed fish. FLX acts as a disruptor of various neuroendocrine functions in the brain, but nothing is known about the possible consequence of FLX exposure on the cardio-ventilatory system in fish. Here we undertook to investigate the central actions of FLX on ventilatory and cardiovascular function in unanesthetized rainbow trout (Oncorhynchus mykiss). Intracerebroventricular (ICV) injection of FLX (dosed between 5 and 25μg) resulted in a significantly elevated total ventilation (VTOT), with a maximum hyperventilation of +176% (at a dose of 25μg) compared with vehicle injected controls. This increase was due to an increase in ventilatory amplitude (VAMP: +126%) with minor effects on ventilatory frequency. The highest dose of FLX (25μg) produced a significant increase in mean dorsal aortic blood pressure (PDA: +20%) without effects on heart rate (ƒH). In comparison, intra-arterial injections of FLX (500–2500μg) had no effect on ventilation but the highest doses increased both PDA and ƒH. The ICV and IA cardio-ventilatory effects of FLX were very similar to those previously observed following injections of 5-HT, indicating that FLX probably acts via stimulating endogenous 5-HT activity through inhibition of 5-HT transporter(s).Our results demonstrate for the first time in fish that FLX administered within the brain exerts potent stimulatory effects on ventilation and blood pressure increase. The doses of FLX given to fish in our study are higher than the brain concentrations of FLX in fish that result from acute exposure to FLX through the water. Nonetheless, our results indicate possible disrupting action of long term exposure to FLX discharged into the environment on central target sites sensitive to 5-HT involved in cardio-ventilatory control.

Central ventilatory and cardiovascular actions of serotonin in trout

This study was undertaken to investigate the central actions of 5-HT on ventilatory and cardiovascular variables in the unanesthetized trout. Compared to vehicle, intracerebroventricular injection (ICV) of 5-HT elevated the total ventilation. This elevation was due to its stimulatory action on ventilatory amplitude. Moreover, 5-HT produced a dose-dependent increase in mean dorsal aortic blood pressure (PDA) without change in heart rate (fH). Methysergide, a 5-HT1/5-HT2 receptor antagonist, reduced the hyperventilatory and hypertensive actions of 5-HT. 8-OH-2-(di-n-propylamino) tetralin, a 5-HT1A receptor agonist, increased PDA while α-methyl-5-HT, a 5-HT2 receptor agonist, elevated all ventilatory variables and increased PDA without changing fH. Intra-arterial injection of 5-HT was without effect on ventilation, but 5-HT initially produced hypotension followed by hypertension. These changes were accompanied by tachycardia. It remains to be determined whether endogenous 5-HT within the brain of trout may act as a potent neuroregulator causing stimulatory effects on cardio-ventilatory functions. In the periphery, 5-HT may act as local modulator involved in vasoregulatory mechanisms.

Central ventilatory and cardiovascular actions of trout gastrin-releasing peptide (GRP) in the unanesthetized trout

SummaryGastrin-releasing peptide (GRP), a neuropeptide initially isolated from porcine stomach, shares sequence similarity with bombesin. GRP and its receptors are present in the brains and peripheral tissues of several species of teleost fish, but little is known about the ventilatory and cardiovascular effects of this peptide in these vertebrates. The goal of this study was to compare the central and peripheral actions of picomolar doses of trout GRP on ventilatory and cardiovascular variables in the unanesthetized rainbow trout. Compared to vehicle, intracerebroventricular (ICV) injection of GRP (1–50 pmol) significantly elevated the ventilation rate (ƒV) and the ventilation amplitude (VAMP), and consequently the total ventilation (VTOT). The maximum hyperventilatory effect of GRP (VTOT: +225%), observed at a dose of 50 pmol, was mostly due to its stimulatory action on VAMP (+170%) rather than ƒV (+20%). In addition, ICV GRP (50 pmol) produced a significant increase in mean dorsal aortic blood pressure (PDA) (+35%) and in heart rate (ƒH) (+25%). Intra-arterial injections of GRP (5–100 pmol) were without sustained effect on the ventilatory variables but produced sporadic and transient increases in ventilatory movement at doses of 50 and 100 pmol. At these doses, GRP elevated PDA by +20% but only the 50 pmol dose significantly increased HR (+15%). In conclusion, our study suggests that endogenous GRP within the brain of the trout may act as a potent neurotransmitter and/or neuromodulator in the regulation of cardio-ventilatory functions. In the periphery, endogenous GRP may act as locally-acting and/or circulating neurohormone with an involvement in vasoregulatory mechanisms.

Central ventilatory and cardiovascular actions of angiotensin peptides in trout

In the brains of teleosts, angiotensin II (ANG II), one of the main effector peptides of the renin-angiotensin system, is implicated in various physiological functions notably body fluid and electrolyte homeostasis and cardiovascular regulation, but nothing is known regarding the potential action of ANG II and other angiotensin derivatives on ventilation. Consequently, the goal of the present study was to determine possible ventilatory and cardiovascular effects of intracerebroventricular injection of picomole doses (5-100 pmol) of trout [Asn(1)]-ANG II, [Asp(1)]-ANG II, ANG III, ANG IV, and ANG 1-7 into the third ventricle of unanesthetized trout. The central actions of these peptides were also compared with their ventilatory and cardiovascular actions when injected peripherally. Finally, we examined the presence of [Asn(1)]-ANG II, [Asp(1)]-ANG II, ANG III, and ANG IV in the brain and plasma using radioimmunoassay coupled with high-performance liquid chromatography. After intracerebroventricular injection, [Asn(1)]-ANG II and [Asp(1)]-ANG II two ANG IIs, elevated the total ventilation through a selective stimulatory action on the ventilation amplitude. However, the hyperventilatory effect of [Asn(1)]-ANG II was threefold higher than the effect of [Asp(1)]-ANG II at the 50-pmol dose. ANG III, ANG IV, and ANG 1-7 were without effect. In addition, ANG IIs and ANG III increased dorsal aortic blood pressure (P(DA)) and heart rate (HR). After intra-arterial injections, none of the ANG II peptides affected the ventilation but [Asn(1)]-ANG II, [Asp(1)]-ANG II, and ANG III elevated P(DA) (50 pmol: +80%, +58% and +48%, respectively) without significant decrease in HR. In brain tissue, comparable amounts of [Asn(1)]-ANG II and [Asp(1)]-ANG II were detected (ca. 40 fmol/mg brain tissue), but ANG III was not detected, and the amount of ANG IV was about eightfold lower than the content of the ANG IIs. In plasma, ANG IIs were also the major angiotensins (ca. 110 fmol/ml plasma), while significant but lower amounts of ANG III and ANG IV were present in plasma. In conclusion, our study suggests that the two ANG II isoforms produced within the brain may act as a neurotransmitter and/or neuromodulator to regulate the cardioventilatory functions in trout. In the periphery, two ANG IIs and their COOH-terminal peptides may act as a circulating hormone preferentially involved in cardiovascular regulations.

Central ventilatory and cardiovascular actions of calcitonin gene-related peptide in unanesthetized trout

Calcitonin gene-related peptide (CGRP) and its receptors are widely distributed in the tissues of teleost fish, including the brain, but little is known about the ventilatory and cardiovascular effects of the peptide in these vertebrates. The present study was undertaken to compare the central and peripheral actions of graded doses (5-50 pmol) of trout CGRP on ventilatory and cardiovascular variables in unanesthetized rainbow trout. Compared with vehicle, intracerebroventricular injection of CGRP significantly elevated the ventilation frequency (f(V)) and the ventilation amplitude (V(AMP)) and, consequently, the total ventilation (V(TOT)). The maximum hyperventilatory effect of CGRP (V(TOT): +300%), observed at a dose of 50 pmol, was mostly due to its stimulatory action on V(AMP) (+200%) rather than f(V) (+30%). In addition, CGRP produced a significant and dose-dependent increase in mean dorsal aortic blood pressure (P(DA)) (50 pmol: +40%) but the increase in heart rate (f(H)) was not significant. Intra-arterial injections of CGRP were without effect on the ventilatory variables but significantly and dose-dependently elevated P(DA) (50 pmol: +36%) without changing f(H). At the highest dose tested, this hypertensive phase was preceded by a rapid and transient hypotensive response. In conclusion, our study suggests that endogenous CGRP within the brain of the trout may act as a potent neurotransmitter and/or neuromodulator in the regulation of cardio-ventilatory functions. In the periphery, endogenous CGRP may act as a local and/or circulating hormone preferentially involved in vasoregulatory mechanisms.

Hypoxia tolerance in elasmobranchs. II. Cardiovascular function and tissue metabolic responses during progressive and relative hypoxia exposures

Cardiovascular function and metabolic responses of the heart and other tissues during hypoxia exposure were compared between the hypoxia-tolerant epaulette shark (Hemiscyllium ocellatum) and the hypoxia-sensitive shovelnose ray (Aptychotrema rostrata). In both species, progressive hypoxia exposure caused increases in stroke volume and decreases in heart rate, cardiac output, cardiac power output (CPO, an assessment of cardiac energy demand) and dorsal aortic blood pressure, all of which occurred at or below each species' critical P(O2) for whole-animal O(2) consumption rate, M(O2) (P(crit)). In epaulette sharks, which have a lower P(crit) than shovelnose rays, routine levels of cardiovascular function were maintained to lower water P(O2) levels and the changes from routine levels during hypoxia exposure were smaller compared with those for the shovelnose ray. The maintenance rather than depression of cardiovascular function during hypoxia exposure may contribute to the superior hypoxia tolerance of the epaulette shark, presumably by improving O(2) delivery and waste removal. Compared with shovelnose rays, epaulette sharks were also better able to maintain a stable cardiac high-energy phosphate pool and to minimize metabolic acidosis and lactate accumulation in the heart (despite higher CPO) and other tissues during a 4 h exposure to 40% of their respective P(crit) (referred to as a relative hypoxia exposure), which results in similar hypoxaemia in the two species (∼16% Hb-O(2) saturation). These different metabolic responses to relative hypoxia exposure suggest that variation in hypoxia tolerance among species is not solely dictated by differences in O(2) uptake and transport but also by tissue-specific metabolic responses. In particular, lower tissue [lactate] accumulation in epaulette sharks than in shovelnose rays during relative hypoxia exposure suggests that enhanced extra-cardiac metabolic depression occurs in the former species. This could facilitate strategic utilization of available O(2) for vital organs such as the heart, potentially explaining the greater hypoxic cardiovascular function of epaulette sharks.

Ventilatory and cardiovascular actions of centrally and peripherally administered trout pituitary adenylate cyclase-activating polypeptide (PACAP) and vasoactive intestinal peptide (VIP) in the unanaesthetized trout

In mammals, pituitary adenylate cyclase-activating polypeptide (PACAP) and vasoactive intestinal peptide (VIP) are involved in cardiovascular and respiratory regulation. Several studies have demonstrated the presence of PACAP, VIP and their receptors in various tissues of teleost fish, including the brain, but little is known about their respiratory and cardiovascular effects. The present study was undertaken to compare the central and peripheral actions of graded doses (25-100 pmol) of trout PACAP and trout VIP on ventilatory and cardiovascular variables in the unanaesthetized rainbow trout. Compared with vehicle, only intracerebroventricular injection of PACAP significantly (P<0.05) elevated the ventilation frequency and the ventilation amplitude, but both peptides significantly increased the total ventilation (total ventilation). However, the maximum hyperventilatory effect of PACAP was approximately 2.5-fold higher than the effect of VIP at the 100 pmol dose (PACAP, (total ventilation)=+5407+/-921 arbitrary units, a.u.; VIP, (total ventilation)=+2056+/-874 a.u.; means +/- s.e.m.). When injected centrally, only PACAP produced a significant increase in mean dorsal aortic blood pressure (P(DA)) (100 pmol: +21%) but neither peptide affected heart rate (f(H)). Intra-arterial injections of either PACAP or VIP were without effect on the ventilatory variables. PACAP was without significant action on P(DA) and f(H) while VIP significantly elevated P(DA) (100 pmol: +36%) without changing f(H). In conclusion, the selective central hyperventilatory actions of exogenously administered trout PACAP, and to a lesser extent VIP, suggest that the endogenous peptides may be implicated in important neuroregulatory functions related to the central control of ventilation in trout.

The effects of acute changes in temperature and oxygen availability on cardiac performance in winter flounder (Pseudopleuronectes americanus)

Studies on how flatfish cardiovascular function responds to environmental challenges are limited, and have largely relied upon indirect methodologies (i.e. Fick principle). Thus, we measured dorsal aortic blood pressure (P(DA)) and cardiac function in 8 and 15 degrees C-acclimated flounder exposed to graded hypoxia, and in 8 degrees C-acclimated fish exposed to an acute temperature increase to their critical thermal maximum (CTM). The extent of bradycardia in 8 degrees C-acclimated fish (decrease in heart rate of 41%) was consistent with that observed for other teleosts, as was this species' CTM (25.8+/-0.5 degrees C) and its cardiac response to increasing temperature. However, this study provides further examples of how cardiovascular function is controlled differently in the flounder as compared with other fishes. First, the onset of bradycardia in 8 degrees C-acclimated fish occurred earlier than expected for this inactive and hypoxia-tolerant species (60% water air saturation). Second, resting cardiac output was similar in flounder acclimated to 8 and 15 degrees C (approximately 15 mL min(-1) kg(-1)), and hypoxic bradycardia was surprisingly absent at 15 degrees C. Finally, systemic vascular resistance decreased when flounder were exposed to elevated temperature, and this resulted in a 26% fall in P(DA). These are novel findings, however, the extent to which the flounder's behaviour influenced some of the results is unclear.

Sex-specific differences in cardiac control and hematology of sockeye salmon (Oncorhynchus nerka) approaching their spawning grounds

Some male salmonids (e.g., rainbow trout) display profound cardiovascular adjustments during sexual maturation, including cardiac growth and hypertension, and tachycardia has been observed in free-ranging male salmonids near their spawning grounds. In the present study, we investigated cardiac control, dorsal aortic blood pressure, cardiac morphometrics, and hematological variables in wild, sexually maturing sockeye salmon (Oncorhynchus nerka) with a particular aim to decipher any sex-specific differences. Routine heart rate (f(H)) was significantly higher in females (52 vs. 43 beats/min), which was due to significantly lower cholinergic tone (28 vs. 46%), because there were no differences in adrenergic tone or intrinsic heart rate between sexes. No differences in blood pressure were observed despite males possessing an 11% greater relative ventricular mass. Concomitant with higher routine heart rates, female sockeye had significantly higher levels of cortisol, testosterone, and 17beta-estradiol, whereas the level of 11-ketotestosterone was higher in males. There were no differences in hematocrit or hemoglobin concentration between the sexes. The findings of this study highlight the importance of considering sex as a variable in research fields such as conservation biology and when modeling the consequences of local and global climate change. Indeed, this study helps to provide a mechanistic basis for the significantly higher rates of female mortality observed in previous studies of wild-caught sockeye salmon.

Central and Peripheral Cardiovascular Effects of Angiotensin III in Trout

The present study was undertaken to determine the central and peripheral actions of trout angiotensin III (ANG III) on heart rate (HR) and mean dorsal aortic blood pressure (P(DA)) in the unanaesthetized rainbow trout. Intracerebroventricular injection of ANG III (5-100 pmol) produced a significant and dose-dependent increase in HR without significant change in P(DA). In contrast, when injected peripherally ANG III (5-50 pmol) evoked a significant and dose-dependent increase in P(DA). The hypertensive responses were accompanied by a bradycardia that reached significance only for the highest dose of ANG III tested. In conclusion, our results have shown that ANG III has potent and contrasting cardiovascular actions depending on whether its site of action is the brain or the peripheral circulation. Endogenous ANG III may have important physiological functions in teleost fishes.

Effects of gastric distension and feeding on cardiovascular variables in the shorthorn sculpin (Myoxocephalus scorpius)

We have previously shown in rainbow trout (Oncorhynchus mykiss) that gastric distension induces an instantaneous alpha-adrenoceptor-mediated increase in the dorsal aortic blood pressure (P(da)), with no change in cardiac output (CO), gut blood flow (Q(cma)), or heart rate. To investigate if feeding habits affect these patterns and to compare the differences between gastric distension alone and feeding in the same experimental setting, we used the short-horn sculpin (Myoxocephalus scorpius), an inactive ambush predator with a capacity to eat large meals. An inflatable balloon was placed in the stomach of one group while another group was fed fish meat. When distending the stomach with a volume corresponding to a meal of 8-10% body weight, there is a profound and long-lasting increase in systemic (123 +/- 27%) and gastrointestinal (R(cma); 82 +/- 24%) vascular resistance, leading to an increase in P(da) (19%) without any change in CO or Q(cma). After force-feeding, there is a rapid transient increase in R(cma) (24 +/- 4%) and an even larger P(da) response (53%). There is also a subsequent increase in both CO (28 +/- 8%) and Q(cma) (27 +/- 9%) after 30 min. By 15 h, CO and Q(cma) increase further (41 +/- 11 and 63 +/- 14%, respectively), and this increase persists for up to 60 h. The increase in Q(cma) is mediated via both an increase in CO and a shunting of blood from the systemic circulation via a decrease in R(cma) (34 +/- 7%). In conclusion, the response to mechanical distension of the stomach is similar to what we have described in rainbow trout, and the postprandial gastrointestinal hyperemia is most likely chemically induced.

Circulatory limits to oxygen supply during an acute temperature increase in the Chinook salmon (Oncorhynchus tshawytscha)

This study was undertaken to provide a comprehensive set of data relevant to disclosing the physiological effects and possible oxygen transport limitations in the Chinook salmon (Oncorhynchus tshawytscha) during an acute temperature change. Fish were instrumented with a blood flow probe around the ventral aorta and catheters in the dorsal aorta and sinus venosus. Water temperature was progressively increased from 13 degrees C in steps of 4 degrees C up to 25 degrees C. Cardiac output increased from 29 to 56 ml.min(-1).kg(-1) between 13 and 25 degrees C through an increase in heart rate (58 to 105 beats/min). Systemic vascular resistance was reduced, causing a stable dorsal aortic blood pressure, yet central venous blood pressure increased significantly at 25 degrees C. Oxygen consumption rate increased from 3.4 to 8.7 mg.min(-1).kg(-1) during the temperature increase, although there were signs of anaerobic respiration at 25 degrees C in the form of increased blood lactate and decreased pH. Arterial oxygen partial pressure was maintained during the heat stress, although venous oxygen partial pressure (Pv(O(2))) and venous oxygen content were significantly reduced. Cardiac arrhythmias were prominent in three of the largest fish (>4 kg) at 25 degrees C. Given the switch to anaerobic metabolism and the observation of cardiac arrhythmias at 25 degrees C, we propose that the cascade of venous oxygen depletion results in a threshold value for Pv(O(2)) of around 1 kPa. At this point, the oxygen supply to systemic and cardiac tissues is compromised, such that the oxygen-deprived and acidotic myocardium becomes arrhythmic, and blood perfusion through the gills and to the tissues becomes compromised.

Enforced exercise, but not acute temperature elevation, decreases venous capacitance in the stenothermal Antarctic fish Pagothenia borchgrevinki

The venous haemodynamic response to enforced exercise and acute temperature increase was examined in the Antarctic fish Pagothenia borchgrevinki (borch) to enable comparisons with the existing literature for temperate species, and investigate if the unusual cardiovascular response to temperature changes previously observed in the borch can be linked to an inability to regulate the venous vasculature. Routine central venous blood pressure (P (cv)) was 0.08 kPa and the mean circulatory filling pressure (P (mcf); an index of venous capacitance) was 0.14 kPa. Acute warming from 0 to 2.5 and 5 degrees C increased heart rate (f (H)), while dorsal aortic blood pressure (P (da)) decreased. P (mcf) did not change, while P (cv) decreased significantly at 5 degrees C. This contrasts with the venoconstriction previously observed in rainbow trout in response to increased temperature. Exercise resulted in small increases in P (mcf) and P (cv), a response that was abolished by alpha-adrenoceptor blockade. This study demonstrates that the heart of P. borchgrevinki normally operates at positive filling pressures (i.e. P (cv)) and that venous capacitance can be actively regulated by an alpha-adrenergic mechanism. The lack of decrease in venous capacitance during warming may suggest that a small increase in venous tone is offset by a passive temperature-mediated increase in compliance.

Effects of gastric distension on the cardiovascular system in rainbow trout (Oncorhynchus mykiss)

When animals feed, blood flow to the gastrointestinal tract increases to ensure an adequate oxygen supply to the gastrointestinal tissue and an effective absorption of nutrients. In mammals, this increase depends on the chemical properties of the food, as well as, to some extent, on the mechanical distension of the stomach wall. By using an inflatable nitrile balloon positioned in the stomach, we investigated the cardiovascular responses to mechanical stretch of the stomach wall in rainbow trout (Oncorhynchus mykiss). Distension with a volume equivalent to a meal of 2% of the body mass increased dorsal aortic blood pressure by up to 29%, and central venous blood pressure increased transiently nearly fivefold. The increase in arterial pressure was mediated by an increased vascular resistance of both the systemic and the intestinal circulation. Cardiac output, heart rate, and stroke volume (SV) did not change, and only transient changes in gut blood flow were observed. The increase in arterial pressure was abolished by the alpha-adrenergic antagonist prazosin, indicating an active adrenergic vasoconstriction, whereas the venous pressor response could be the consequence of a passive increase in intraperitoneal pressure. Our results show that mechanical distension of the stomach causes an instantaneous increase in general vascular resistance, which may facilitate a redistribution of blood to the gastrointestinal tract when chemical stimuli from a meal induce vasodilation in the gut circulation. The normal postprandial increase in gut blood flow in teleosts is, therefore, most likely partly dependent on mechanical stimuli, as well as on chemical stimuli.

Ventilatory and cardiovascular actions of centrally administered trout tachykinins in the unanesthetized trout

The brains of teleost fish contain members of the tachykinin family that are the products of orthologous genes expressed in mammalian nervous tissues, but little is known regarding the physiological effects of these peptides in their species of origin. The present study compares the central actions of trout neuropeptide gamma (NPgamma), substance P (SP) and neurokinin A (NKA) (5-250 pmol) on ventilatory and cardiovascular parameters in the unanesthetized rainbow trout Oncorhynchus mykiss. Intracerebroventricular (ICV) injection of NPgamma evoked a dose-dependent elevation of the ventilation rate (f(V)) but a reduction of the ventilation amplitude (V(AMP)) that was caused by a reduction of the magnitude of the adduction phase of the ventilatory signal. The net effect of NPgamma was to produce an hypoventilatory response since the total ventilation (V(TOT)) was significantly reduced. The minimum effective dose for a significant effect of NPgamma on f(V) and V(AMP) was 50 pmol. SP evoked a significant elevation of f(V), a concomitant depression of V(AMP), and a resultant decrease in V(TOT) but only at the highest dose (250 pmol). NKA was without action on f(V) but significantly decreased V(AMP) at only the highest dose tested. In this case also, the net effect of NKA was to reduce V(TOT). When injected centrally, none of the three peptides, at any dose tested, produced changes in heart rate or mean dorsal aortic blood pressure (P(DA)). Intra-arterial injection of the three tachykinins (250 pmol) produced a significant (P<0.05) increase in P(DA), but only SP and NKA induced concomitant bradycardia. None of the three peptides produced any change in f(V) or V(AMP). In conclusion, our results demonstrate that centrally injected tachykinins, particularly NPgamma, produce a strong hypoventilatory response in a teleost fish and so suggest that endogenous tachykinins may be differentially implicated in neuroregulatory control of ventilation.

Stanniectomy attenuates the renin–angiotensin response to hypovolemic hypotension in freshwater eels (Anguilla rostrata) but not blood pressure recovery

Plasma Angiotensin II (ANG II) concentrations were measured in SHM (sham-operated 2 weeks) and CSX (corpuscles of Stannius removed 2 weeks) eels before and after the induction of hypovolemic hypotension (HH) by the rapid withdrawal of 8 ml kg bw(-1) of caudal venous blood. Baseline (before exsanguination) plasma ANG II concentrations were similar in SHM and CSX eels (81.3 +/- 18.8 fmol ml(-1) cf. 106 +/- 31.6 fmol ml(-1), respectively) but the elevation in plasma ANG II following HH (1,732 +/- 82 fmol ml(-1)) was attenuated by CSX (368 +/- 127 fmol ml(-1)) showing that the CS are linked to plasma ANG II concentrations. Plasma ANG II in both groups returned to baseline levels within 48 h. Dorsal aortic blood pressures (DABP) were measured in both experimental groups before, and during the 60 min after, blood withdrawal. A 44% decrease in mean DABP was observed in both SHM and CSX eels within 2 min and followed by similar rapid patterns of recovery of systolic, diastolic, and pulse pressures in both groups during the next 60 min showing that short-term recovery of DABP is not CS-dependent. Stanniectomy increased plasma Ca and K(+) and decreased plasma Mg, Na(+), Cl(-) and osmolality which confirms some earlier observations in eels and other freshwater teleosts.

Cardiovascular changes under normoxic and hypoxic conditions in the air-breathing teleostSynbranchus marmoratus: importance of the venous system

Synbranchus marmoratus is a facultative air-breathing fish, which uses its buccal cavity as well as its gills for air-breathing. S. marmoratus shows a very pronounced tachycardia when it surfaces to air-breathe. An elevation of heart rate decreases cardiac filling time and therefore may cause a decline in stroke volume (V(S)), but this can be compensated for by an increase in venous tone to maintain stroke volume. Thus, the study on S. marmoratus was undertaken to investigate how stroke volume and venous function are affected during air-breathing. To this end we measured cardiac output (Q), heart rate (f(H)), central venous blood pressure (P(CV)), mean circulatory filling pressure (MCFP), and dorsal aortic blood pressures (P(DA)) in S. marmoratus. Measurements were performed in aerated water (P(O2)>130 mmHg), when the fish alternated between gill ventilation and prolonged periods of apnoeas, as well as during hypoxia (P(O2)<or=50 mmHg), when the fish changed from gill ventilation to air-breathing. Q increased significantly during gill ventilation compared to apnoea in aerated water through a significant increase in both f(H) and V(S). P(CV) and MCFP also increased significantly. During hypoxia, when the animals surface to ventilate air, we found a marked rise in f(H), P(CV), MCFP, Q and V(S), whereas P(DA) decreased significantly. Simultaneous increases in P(CV) and MCFP in aerated, as well as in hypoxic water, suggests that the venous system plays an important regulatory role for cardiac filling and V(S) in this species. In addition, we investigated adrenergic regulation of the venous system through bolus infusions of adrenergic agonists (adrenaline, phenylephrine and isoproterenol; 2 microg kg(-1)). Adrenaline and phenylephrine caused a marked rise in P(CV) and MCFP, whereas isoproterenol led to a marked decrease in P(CV), and tended to decrease MCFP. Thus, it is evident that stimulation of both alpha- and beta-adrenoreceptors affects venous tone in S. marmoratus.