Depressor Nerve Research Articles

Positive End-Expiratory Pressure Ventilation Elicits Increases in Endogenously Formed Nitric Oxide as Detected in Air Exhaled by Rabbits

Nitric oxide (NO) formed from L-arginine is exhaled by mammals and regulates pulmonary vascular tone. Little is known about how its formation is stimulated. The concentration of NO in exhaled air was monitored by chemiluminescence in pentobarbital-anesthetized rabbits receiving mechanical ventilation by tracheostomy with graded positive end-expiratory pressure (PEEP). Introduction of PEEP (2.5-15 cmH2O) elicited dose-dependent and reproducible increments in exhaled NO and in arterial oxygen tension (PaO2). The increase in exhaled NO exhibited a biphasic pattern, with an initial peak followed by a partial reversal during the 4-min period at each level of PEEP. Thus, at a PEEP of 10 cmH2O, exhaled NO initially increased from 19 +/- 4 to 30 +/- 5 parts per billion (ppb) (P < 0.001, n = 9) and then decreased to 27 +/- 5 ppb (P < 0.005) at the end of the 4-min observation period. Simultaneously, PaO2 increased from 75 +/- 12 mmHg in the control situation to 105 +/- 11 mmHg (P < 0.05) at a PEEP of 10 cmH2O. After bilateral vagotomy, including bilateral transection of the depressor nerves, the increase in exhaled NO in response to PEEP was significantly reduced (P < 0.01). Thus, after vagotomy, a PEEP of 10 cmH2O elicited an increase in the concentration of exhaled NO from 13 +/- 3 to 17 +/- 3 ppb (n = 7). Vagotomy did not affect the baseline concentration of NO in exhaled air. The PEEP-induced increments in PaO2 were not affected by the NO synthase inhibitor L-N omega-arginine-methylester (30 mg.kg-1 intravenously). In open-chest experiments, PEEP (10 cmH2O) induced a reduction in cardiac output from 317 +/- 36 to 235 +/- 30 ml.min-1 and an increase in exhaled NO from 23 +/- 6 to 30 +/- 7 ppb (P < 0.05, n = 5). Reduction in cardiac output from 300 +/- 67 to 223 +/- 52 ml.min-1 by partial obstruction of the pulmonary artery did not significantly increase exhaled NO (from 23 +/- 7 to 25 +/- 6, difference not significant; n = 3). PEEP elicited increments in exhaled NO, perhaps by a stretch-dependent effect on the respiratory system. This finding may be attributed in part to a vagally influenced mechanism.

Abdominal vagal stimulation excites bulbospinal barosensitive neurons in the rostral ventrolateral medulla

We used extracellular recordings to examine the central pathway whereby electrical stimulation of abdominal vagal afferents elevates arterial pressure in the rabbit. Bulbospinal neurons in the rostral ventrolateral medulla were identified by antidromic activation from the dorsolateral funiculus of the thoracic spinal cord. Their barosensitivity was assessed by their response to intravenous phenylephrine and by their cardiac cycle-related rhythmicity. We used peristimulus histogram procedures to assess the effect of electrical stimulation of abdominal vagal afferents on the discharge rate of these neurons. Electrical stimulation (one to three pulses) activated 98 of 123 neurons tested (80%), had no effect on 22 neurons (18%) and inhibited the remaining three neurons. Latency to peak excitation was 228 +/- 3 ms, indicating that the conduction velocity of the vagal afferents was about 0.6 m/s, in the unmyelinated fibre range. Lower oesophageal distension with a balloon excited 22 of 48 neurons (46%), inhibited 12 neurons (25%) and had no effect on the remaining 14 cells (29%). Vagally induced excitation was reduced by aortic depressor nerve stimulation in nine of 13 neurons. Lightly touching the animal's back and legs had no effect on 56 of 60 neurons. Nociceptive stimuli failed to affect 47 of 60 neurons tested. No excitation was seen with electrical stimulation of the sciatic or central ear nerves. Our study identifies a robust excitatory input from the abdominal vagus to bulbospinal barosensitive neurons in the rostral ventrolateral medulla. Relevant physiological stimuli include lower oesophageal distension. The pathways may be relevant to cardiovascular changes which accompany upper gastrointestinal function.

Daily spontaneous running attenuated the central gain of the arterial baroreflex.

Exercise training attenuates arterial baroreflex function. Mechanisms responsible may include an attenuated aortic baroreceptor reactivity (afferent mechanisms) and/or an attenuated central baroreflex gain. We tested the hypothesis that the aortic baroreceptor reactivity and/or central gain is attenuated by daily spontaneous running (DSR). Eighteen anesthetized Sprague-Dawley rats (11 control and 7 DSR) were tracheotomized and instrumented with femoral venous and right carotid arterial catheters. Electrodes were placed around the left aortic depressor nerve and the lumbar sympathetic trunk. Eight to thirteen weeks of DSR were associated with a 20% increase in heart weight-to-body weight ratio (2.83 +/- 0.04 vs. 3.39 +/- 0.10 g/kg; P < 0.001) and resting bradycardia (413 +/- 6 vs. 384 +/- 10 beats/min; P = 0.01). DSR reduced the central gain of the baroreflex regulation of heart rate (0.210 +/- 0.046 vs. 0.005 +/- 0.021 beats.min-1.%-1; P = 0.004) during decreases in arterial pressure. However, the reactivity of aortic baroreceptor afferents and the central gain of the baroreflex control of lumbar sympathetic nerve activity were not different in control and DSR rats. Thus DSR reduced the central gain of the arterial baroreflex regulation of heart rate without changing the reactivity of aortic baroreceptor afferents. We conclude that afferent mechanisms are not responsible for the training-induced reduction in arterial baroreflex function.

Cardiorespiratory reflex control in rats with left ventricular dysfunction.

Patients with heart failure exhibit a neurohumoral excitatory state and abnormal baroreflex control of the cardiovascular system. We determined whether arterial baroreflexes are impaired during left ventricular dysfunction (LVD) caused by chronic myocardial infarction in the absence of congestive heart failure and whether abnormal central mechanisms contribute to this impairment. Baroreceptors were stimulated in anesthetized rats with and without LVD by increasing arterial pressure with phenylephrine. Lumbar sympathetic nerve and phrenic nerve activity as well as heart rate were recorded. Rats were divided into different groups based on infarct size. Rats with moderate LVD showed impaired baroreflex control of sympathetic, ventilatory, and heart rate responses. Baroreflex gains were inversely related to the size of the infarct. The central gain for sympathetic nerve activity, obtained by using electrical stimulation of the aortic depressor nerve, also was impaired. Baroreflex control of the cardiorespiratory system is thus impaired in rats with moderate LVD in the absence of congestive heart failure. The attenuated baroreflexes are likely due to abnormal afferent mechanisms, although central mechanisms contribute to the impaired barosympathetic reflex.

Learning of physiological responses: II. Classical conditioning of the baroreflex.

The baroreflex can be classically conditioned. In neuromuscular blocked (NMB) rats, electrical stimulation of the aortic depressor nerve (ADN) and dopamine-produced blood pressure rise were effective unconditioned stimuli (UCS) for auditory discriminative classical conditioning. The conditioned response (CR) pattern (bradycardia, vasodilatation, and hypotension > 10 torr) closely resembled that of the unconditioned baroreflex. Conditioned stimulus (CS) specificity was demonstrated by discrimination of baroreflex-associated and nonassociated auditory stimuli, and also by elaborating depressor and pressor CRs to auditory CSs, which respectively had been associated with either baro-afferent (depressor) or tail-shock (pressor) UCSs. The conditioned-baroreflex-magnitude increased with trials. These findings support quantitative models in which CRs interact with and calibrate the gain and dynamic properties of natural reflexes.

Criteria for intracellular identification of pre-sympathetic neurons in the rostral ventrolateral medulla in the rat.

Previous studies revealed that a relatively small group of reticulospinal neurons located in the rostral ventrolateral medulla (RVLM) plays a key role in the generation of resting vasomotor tone and in reflex control of arterial blood pressure. These medullary pre-sympathetic neurons have been extensively studied with extracellular microelectrodes, but so far few attempts have been made to examine their intracellular properties in vivo. This report, based on intracellular recordings from 8 RVLM pre-sympathetic neurons in anaesthetised rats, sets out criteria for intracellular identification of such neurons. We propose that two features are sufficient to classify RVLM neurons as pre-sympathetic during intracellular recording: inhibitory response to stimulation of the aortic depressor nerve with short bursts of pulses applied at low frequency; and antidromic stimulation from the upper thoracic segments. Cardiac oscillations in the membrane potential or responses during large changes in blood pressure can be due to movement artefact, and are therefore not reliable as a means of demonstrating baroreceptor input. Further intracellular studies of these neurons will undoubtedly result in further progress in understanding their function.

Hemodynamics and baroreflex function in rats with nephrotic syndrome

The excess renal sodium retention leading to edema formation in the nephrotic syndrome (NS) is substantially dependent on increased efferent renal sympathetic nerve activity (RSNA). This study examined whether the hypoalbuminemia in NS is reflected as a decrease in cardiac output or cardiac function and whether the increased RSNA in NS is due to alterations in arterial and/or cardiopulmonary baroreflex function. NS was induced in rats with adriamycin (3.5 mg/kg i.v.), and they were studied 4 wk after injection. Mean arterial pressure (MAP) was similar in control (C) and NS rats. Cardiac indexes (CIs; cardiac output/body wt) were 29 +/- 1 and 26 +/- 1 ml.min-1.100 g-1 in C and NS rats, respectively. Total peripheral resistance indexes were significantly greater in NS than in C rats (4.7 +/- 0.2 vs. 4.1 +/- 0.1 mmHg.100 g.min.ml-1). Cardiac function during increases in cardiac filling pressure was not different between C and NS rats. The afferent limb of the arterial baroreflex was assessed by measuring aortic depressor nerve activity (ADNA) while the efferent limb was assessed by measuring RSNA in C and NS rats during increases in MAP. The central component of the arterial baroreflex was assessed from plots of RSNA (output) vs. ADNA (input). Comparisons between C and NS rats before and after vagotomy revealed no differences in the gains of any component of the arterial baroreflex. The cardiopulmonary baroreflex was assessed in a similar manner by measuring afferent vagus nerve activity (VGNA) and efferent RSNA during volume expansion before and after sinoaortic denervation (SAD). Before SAD, gains were similar in C and NS rats. After SAD, gains of the total (-1.59 +/- 0.44 vs. -3.64 +/- 0.65%/mmHg) and the central/efferent limb (-0.26 +/- 0.07 vs. -0.67 +/- 0.14 %/%) were significantly reduced (P < 0.05) in NS compared with C rats while the gain of the afferent limb of the reflex was similar in C and NS rats. These results indicate that NS rats with significant hypoalbuminemia maintain an arterial pressure similar to C rats by increasing total peripheral resistance, which serves to offset the tendency to a lower CI. Arterial baroreflex function in NS does not differ from that in C, but decreased cardiopulmonary baroreflex inhibition of RSNA in NS may contribute to the increased RSNA.

Sustained increases in aortic depressor nerve activity after acute elevation in arterial pressure

Despite the return of mean arterial pressure (MAP) to control levels, aortic depressor nerve activity remains elevated from control levels after sustained phenylephrine-induced increases in MAP in spontaneously hypertensive rats (SHR) (Kenney MJ, Morgan DA, Mark AL: Am J Physiol 1990, 258:H1476-H1481). This suggests that sustained increases in arterial pressure may produce prolonged pressure-induced changes in afferent baroreceptor nerve activity in SHR. However, because phenylephrine can exert an excitatory effect on the aortic arch baroreceptors, the increase in aortic depressor nerve activity might have resulted from a persistent direct effect of phenylephrine. The aim of the current study was to determine whether elevations in MAP induced by aortic occlusion produce increases in aortic depressor nerve activity which persist after the return of MAP to control levels. MAP and aortic depressor nerve activity were recorded before, during and after sustained (15-30 min) periods of aortic occlusion in SHR with intact adrenal glands (n = 18) and in adrenalectomized SHR (n = 10). Control experiments were completed in which the same variables were recorded before, during and after sham aortic occlusion in intact (n = 8) and adrenalectomized (n = 8) SHR. Aortic occlusion increased MAP and aortic depressor nerve activity significantly from control levels. After aortic occlusion and the return of MAP to control levels, aortic depressor nerve activity remained significantly increased in 15 experiments, whereas in three experiments aortic depressor nerve activity was reduced. Aortic depressor nerve activity was increased significantly from control levels after aortic occlusion in adrenalectomized rats. Aortic depressor nerve activity remained unchanged from control levels after sham aortic occlusion in intact and adrenalectomized SHR. Sustained elevations in MAP induce increases in aortic depressor nerve activity in intact and adrenalectomized SHR, which persist after the return of MAP to control levels. These observations suggest that sustained increases in arterial pressure may produce prolonged pressure-induced changes in afferent baroreceptor nerve activity in SHR.

Neural organization of the ventilatory activity in the frog, Rana catesbeiana. I

In order to elucidate the neural basis for lung ventilation in the frog, we have investigated the efferent neural activity to oropharyngeal muscles in the decerebrate, paralyzed, unanesthetized bullfrog, Rana catesbeiana. Efferent motor output was recorded from the mandibular branch of the trigeminal (Vmd), the laryngeal branch of the vagus (Xl), and the main and sternohyoid branches of the hypoglossal nerve (Hm and Hsh, respectively). Two types of rhythmic bursting outputs were observed: (1) a high-frequency, low-amplitude, reciprocal oscillation between Vmd, a buccal levator nerve, and Hsh, a buccal depressor nerve; and (2) a low-frequency, high-amplitude, synchronous bursting of Vmd, Hm, Hsh, and Xl. The first type is inferred to represent fictive oropharyngeal ventilation. The second type of burst was divided into four intervals: (a) augmenting activity of Hsh; (b) activation of Xl with continued activation of Hsh; (c) activation of Vmd and Hm (a buccal levator nerve), continued activation of Xl, and termination of Hsh activity; and (d) warning activity in Vmd and Hm associated with a prominent second wave in Xl. This coordinated activity is inferred to represent fictive pulmonary ventilation because the neurograms in these four intervals correspond closely to EMGs and neurograms recorded in the intact frog during the four phases of pulmonary ventilation, namely, buccal depression, pulmonary expiration, pulmonary inspiration, and glottal closure. Hypercapnia, vagotomy, and cutaneous pinching enhanced the high-amplitude, low-frequency rhythm, but not the low-amplitude, high-frequency oscillation. Lung inflation generally inhibited the former and not the latter, but in some cases lung inflation stimulated pulmonary ventilation. We conclude that oropharyngeal and pulmonary ventilation of the frog are produced by one or, possibly, two intrinsically active generators.

Baroreceptor inhibition of the locus coeruleus noradrenergic neurons

The locus coeruleus is involved in the regulation of blood pressure. The present study was undertaken to address the question of how the blood pressure, in turn, changes the activity of the locus coeruleus neurons via the action of baroreceptors. In chloralose- and urethane-anesthetized rats, the central cut end of the aortic depressor nerve, which does not contain chemoreceptor afferents in this species, was stimulated electrically to excite baroreceptor afferents after bilateral vagotomy and sectioning of the carotid sinus nerve. Single train-pulse stimulation of the aortic depressor nerve provoked the inhibition of ongoing activity in 48% of locus coeruleus neurons tested, but 30% of them responded by excitation with subsequent inhibition. However, when the train-pulse stimulation was repeated with a frequency of 5 Hz, which is close to that of the heartbeat in the rat, all neurons were markedly inhibited. Another series of experiments was conducted in vagotomized and carotid sinus nerve-sectioned rats with intact aortic depressor nerves. When blood pressure was elevated by an intravenous injection of a pressor agent, methoxamine or angiotensin II, or by rapid blood loading, ongoing activities of all locus coeruleus neurons tested were suppressed. In contrast, intravenously injected nitroprusside, a depressor agent, increased the activity of locus coeruleus neurons. In rats with all nerves preserved, rapid blood loading markedly inhibited the activity of these neurons. Such inhibition was partially but significantly attenuated by bilateral sectioning of the aortic depressor nerves. It is concluded that activation of aortic baroreceptors provokes inhibitory or excitatory-inhibitory response in locus coeruleus neurons; phasic activation of the baroreceptor afferents with repetitive train-pulse stimulations at a frequency close to that of the heartbeat produces only inhibition, suggesting that, under natural conditions, the locus coeruleus neurons are tonically inhibited by ongoing input from arterial baroreceptors.

Cardiovascular and single unit responses elicited by stimulation of the islands of Calleja and by changes in arterial pressure

Recent experiments in this laboratory have investigated the distribution of the nuclear protein Fos in the rat brain after unilateral electrical stimulation of the aortic depressor nerve and have revealed intense ipsilateral staining in the islands of Calleja. To test the hypothesis that the islands of Calleja may have a role in cardiovascular control, we tested the effect on arterial pressure and heart rate of microinjection of l-glutamate into the islands of Calleja of the artificially ventilated, urethane anesthetized rat. Microinjection of glutamate into the islands of Calleja resulted in a decrease in arterial pressure (24.5 ± 1.5 mmHg) and heart rate (16.6 ± 1.6 bpm). These responses were eliminated by i.v. injection of propranolol or by transection of the spinal cord at the C 1 level. These results are the first demonstration that the islands of Calleja are involved in mediating cardiovascular reflexes primarily through an influence on sympathetic outflow to the heart and vessels. To determine the effects of increases or decreases of arterial pressure on single unit activity in the islands of Calleja, responses of single units in the islands to i.v injection of phenylephrine or sodium nitroprusside were recorded. Of 87 units recorded from in the islands of Calleja, 40 (46%) responded to phenylephrine and 27 (68%) decreased their firing frequency. Of these 27, 16 (59.3%) increased their firing frequency to administration of nitroprusside. In addition, in 11 (31%) of 35 units recorded from in the islands, glutamate microinjection in the nucleus tractus solitarius decreased the firing frequency in 9 (82%) units. Of these 9 units, 7 also decreased their firing frequency to i.v. phenylephrine and increased their firing frequency to i.v. nitroprusside. These results indicate that neurons in the islands of Calleja influence sympathetic control of arterial pressure and heart rate and that single units in the islands respond to changes in arterial pressure.

Arterial baroreflex inhibition by uterine distension in rats

Arterial baroreflexes are inhibited during activation of some viscero-sensory receptors. The present study was designed to determine whether stimulation of mechanoreceptors of the uterus also inhibits the baroreflex bradycardia (BB). The aortic depressor nerve (ADN) was electrically stimulated to elicit BB in chloralose/urethane-anesthetized, succinylcholine-immobilized, and artificially ventilated rats. Hydraulic distension of the uterus with warm 0.9% NaCl solution was found to suppress BB with a threshold intra-uterine pressure of 25–100 mmHg. The inhibition was variably affected by successive transections of the hypogastric nerve (HgN) and the pelvic nerve (PN). In 6 rats out of the 16 tested, preceding transection of either HgN or PN (HgN, 4; PN, 2) abolished the inhibition, whereas in 8 rats the inhibition was not affected by preceding transection of either nerve but was abolished by subsequent transection of the other nerve (PN, 3; HgN, 5). In 2 rats, preceding HgN or PN section reduced the inhibition and subsequent PN or HgN section completed the withdrawal of the inhibition. Recording study comfirmed that both the HgN and PN contain afferent fibers, signalling mechanoceptive information arising in the uterine wall. Electrical stimulation of the HgN as well as the PN remarkably suppressed the BB. In conclusion, uterine distension suppresses the BB and this inhibition is mediated by afferent fibers running in the HgN and PN with variable contributions among animals. The reflex suppression of BB due to uterine sensory activation may contribute to cardiovascular regulation during parturition.

High calcium diet prevents baroreflex impairment in salt-loaded spontaneously hypertensive rats.

To investigate the role of the sympathetic control mechanism in the antihypertensive effect of dietary calcium supplementation, we examined whether a high calcium diet affected mean arterial pressure, renal sympathetic nerve activity, heart rate, and overall and central properties of the arterial baroreceptor reflex in salt-loaded young spontaneously hypertensive rats (SHR). Six-week-old SHR were fed either a normal (0.66%) or high (8.00%) salt diet with either a normal (1.17%) or high (4.07%) calcium content for 4 weeks. The arterial baroreceptor reflex was elicited with rats under halothane anesthesia by altering mean arterial pressure with nitroprusside or phenylephrine. The overall property of the arterial baroreceptor reflex was assessed by the median mean arterial pressure (MAP50) and maximal gain (Gmax) of the relation between mean arterial pressure and renal sympathetic nerve activity and between mean arterial pressure and heart rate. The central property of the arterial baroreceptor reflex was assessed by reflex inhibition of renal sympathetic nerve activity and heart rate elicited by electrical stimulation of the aortic depressor nerve. Compared with the control group fed a normal salt/normal calcium diet, the high salt/normal calcium group had significantly higher mean arterial pressure and renal sympathetic nerve activity but not heart rate. Moreover, the arterial baroreceptor reflex was impaired in the latter group, as evidenced by an increase in MAP50 and decrease in Gmax of the two relations and an attenuation of reflex inhibition of renal sympathetic nerve activity by aortic depressor nerve stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of atropine injected into the nucleus tractus solitarius on the regulation of blood pressure

Previous experiments have demonstrated that stimulation of muscarinic cholinergi receptors in the nucleus tractus solitarius (NTS) of the rat decreases arterial blood pressure and heart rate. The present studies were designed to examine the role of cholinergic mechanisms in the NTS in the tonic regulation of arterial pressure and the baroreceptor reflex. Atropine injected into the NTS of chloralose-anesthetized rats produced a dose-dependent inhibition of cardiovascular responses elicited by injection of acetylcholine into the same site; 240 pmol atropine eliminated acetylcholine-evoked responses. Atropine also increased arterial blood pressure but only at higher doses. Even larger doses of atropine were required to alter cardiovascular responses elicited by electrical stimulation of the aortic depressor nerve. Methylatropine injected into the NTS also blocked acetylcholine-evoked responses but, in contrast to the actions of atropine, did not increase arterial pressure in the dose range required to block acetylcholine-evoked responses. Furthermore, a dose of methylatropine (1 nmol) capable of blocking acetylcholine-evoked cardiovascular responses did not alter aortic depressor nerve-evoked cardiovascular responses. This lack of an effect of methylatropine on arterial pressure and aortic depressor nerve-evoked responses was not due to limited diffusion of the drug within the NTS since 1 nmol methylatropine completely blocked acetylcholine-evoked responses even when injected 0.5 mm distant from the site of acetylcholine injection. These results suggest that cholinergic mechanisms in the NTS are not involved in the tonic regulation of cardiovascular function or the baroreceptor reflex. Furthermore, these results highlight the importance of characterizing doses of drugs used in microinjection studies.

Facilitation of the arterial baroreflex by the ventrolateral part of the midbrain periaqueductal grey matter in rats.

1. The effects of stimulation of the ventrolateral part of the midbrain periaqueductal grey matter (PAG) on the arterial baroreflex were investigated in urethane-chloralose anaesthetized and artificially ventilated rats. 2. Both electrical and chemical stimulation of the ventrolateral PAG provoked hypotension, vagal bradycardia and marked facilitation of baroreflex vagal bradycardia (BVB), which was induced by stimulation of the aortic depressor nerve. The magnitude of ventrolateral PAG facilitation of BVB was 328 +/- 193% (n = 34) for electrical stimulation and 243 +/- 224% (n = 13) for chemical stimulation. Baroreflex hypotension was slightly augmented during either electrical or chemical stimulation of the ventrolateral PAG in vagotomized rats. 3. Stimulation of the nucleus raphe magnus (NRM) also provoked hypotension, vagal bradycardia and facilitation of BVB. The magnitude of BVB facilitation was 234 +/- 132% (n = 8) for electrical stimulation and 328 +/- 170% (n = 7) for chemical stimulation. After microinjection of kainic acid into the NRM region, baroreflex facilitation, as well as hypotension and vagal bradycardia, produced by ventrolateral PAG stimulation, was almost abolished. 4. In conclusion, the ventrolateral PAG, besides producing hypotension and bradycardia, facilitates arterial baroreflexes. These effects are exerted via the NRM, sharply contrasting with effects of the dorsal PAG.

Regulation of plasma vasopressin by plasma osmolality and carotid sinus pressure in anesthetized rabbits.

The purpose of the experiments was to investigate the effect of changes in carotid sinus baroreceptor stimulation on plasma vasopressin (AVP) at different plasma osmolalities in the anesthetized artificially ventilated rabbit. Both carotid sinuses were isolated and perfused with blood at servo-controlled pressures. The vagus and aortic depressor nerves were sectioned bilaterally to eliminate input from atrial and aortic arch baroreceptors. Saline (0.3%, wt/vol) was infused to lower plasma osmolality, and 5% saline was infused to raise plasma osmolality. At three plasma osmolalities, the carotid sinus pressure (CSP) was changed from 100 mmHg to 40 and 140 mmHg and returned to 100 mmHg. There were no changes in plasma AVP in response to changes in CSP at low plasma osmolality (289 mosmol/kgH2O), but at medium (309 mosmol/kgH2O) and high (323 mosmol/kgH2O) osmolality, plasma AVP was higher at 40 than at 140 mmHg CSP. The relationship between plasma AVP and plasma osmolality was expressed as a linear regression at each CSP. Changes in CSP changed the sensitivity but not the threshold of the osmotic control of AVP release.

Effects of scaphognathite nerve stimulation on the acutely deafferented crab ventilatory central pattern generator.

1. Sensory axons from crab (Carcinus maenas) scaphognathites enter the thoracic ganglion primarily via the LNb branch of the levator nerve. The LNa branch of the levator nerve and the depressor nerve each contain relatively few sensory axons. 2. Acutely deafferented ventilatory central pattern generators show a free running burst rate which is lower than that observed in intact crabs. Electrical stimulation of the levator nerve, or of its LNb branch, increases the burst rate in a frequency dependent manner. Stimulation at high enough intensity to recruit afferents will restart a paused motor rhythm. Stimulation of the levator nerve with short pulse trains phase resets and can entrain the rhythm. 3. In addition to increasing the burst rate, LNb stimulation also causes a progressive elimination of motor neurons from the bursts as the stimulating frequency increases, probably due to depolarization of the 3 oval organ 'giant' afferent axons in this branch. Intracellular depolarization of single oval organ afferents will also inhibit some motor neurons as well as slow or stop the rhythm. 4. Continuous stimulation of the depressor nerve does not affect the ganglionic burst rate and this nerve contains only a few small diameter afferent axons; however, brief trains of stimuli can reset the rhythm in a phase-dependent manner.

Effects of Isoflurane on Regulation of Capacitance Vessels under Normotensive and Chronically Hypertensive Conditions

This chapter summarizes several studies that demonstrate that significant differences exist in the reflex regulation of mesenteric capacitance veins in chronic renal wrap hypertensive versus normotensive rabbits. The heart rate response to aortic depressor nerve stimulation and to graded hypoxia has also been equally attenuated by isoflurane in both groups of animals. The two groups of animals also differ significantly in the baseline responses to isoflurane administration. In both groups of animals, 1.5% inhaled isoflurane significantly reduces heart rate and mean arterial pressure and dilated mesenteric capacitance vein diameter. However, in the hypertensive animals, the isoflurane-mediated reduction in arterial pressure has been significantly greater and the isoflurane-mediated increase in mesenteric vein diameter has been significantly less than that observed in the normotensive animals. The present study of the interaction between a volatile anesthetic and the hypertensive condition focused on changes in reflex responses that are mediated primarily by an elevation of sympathetic neural efferent activity. It has been observed that an inhibition of baroreflex and chemoreflex changes in heart rate, blood pressure, and mesenteric vein diameter during the administration of 0.75 minimum alveolar concentration (MAC) isoflurane in normotensive control animals. In addition, isoflurane has been shown to inhibit the relaxation effect of endothelium-derived nitric oxide on vascular smooth muscle cells in in vitro mesenteric vein ring preparations. In the hypertensive animals, the inhibitory effect of isoflurane on the heart rate responses to chemoreflex activation, on the blood pressure responses to both baroreflex and chemoreflex activation and on the mesenteric venodilation in response to aortic depressor nerve stimulation has been the same as in the normotensive control animals. Finally, it should be noted that the action of different anesthetic agents on sympathetically mediated reflex responses, particularly reflex regulation of venous tone, may vary.

Effect of Volatile Anesthetics on Baroreflex Control of Mesenteric Venous Capacitance

Publisher Summary This chapter demonstrates that inhaled anesthetics impede the reflex ability of mesenteric veins to actively constrict and dilate in reaction to baroreflex stimulation. Inhaled anesthetics depress mean arterial pressure, heart rate, and sympathetic efferent outflow. Both low and high doses of inhaled anesthetics attenuate the reflex constriction of mesenteric veins caused by lowered carotid sinus pressure, whereas reflex dilation in response to aortic depressor nerve stimulation has been reduced by the higher dose of inhaled anesthetics. Furthermore, volatile anesthetics dramatically reduce the reflex increase in sympathetic efferent nerve activity as a result of baroreceptor stimulation. On the other hand, direct celiac sympathetic postganglionic activation of the mesenteric veins has been unaffected by even the highest dose of inhaled anesthetics. These findings support the hypothesis that volatile anesthetics may influence mesenteric vascular capacitance through inhibition of the active sympathetic control of veins. An active change in venous capacitance is to be distinguished from a passive reduction of arterial inflow or a redistribution of blood among vascular beds. In situ studies of the differential effects of α1– and α2–adrenoceptor activation on the constriction of mesenteric arteries demonstrate the predominance of α1–receptors in response to endogenous electric stimulation of the celiac ganglion and exogenous application of phenylephrine. The present studies have contributed new evidence from direct observation of the mesenteric veins, indicating that anesthetics inhibit baroreflex regulation of vein diameter and subsequent changes in intravenous pressure, and that the capacitance of the mesenteric bed is, thereby increased.

Transfer function analysis from arterial baroreceptor afferent activity to renal nerve activity in rabbits

In vagotomized and anesthetized rabbits, aortic pressure (AP), aortic depressor nerve activity (ANA), and renal sympathetic nerve activity (RNA) were simultaneously measured while perturbing AP randomly. To quantitatively characterize the role of the arterial baroreflex system in generating RNA, we determined the transfer function (TF) of the central baroreflex arc from ANA to RNA in the frequency domain (0.02-5 Hz). The magnitude of squared coherence was > 0.5, the phase was close to -180 degrees, and the gain of TF was flat over 0.02-0.3 Hz, indicating that changes in RNA were linearly and instantaneously but inversely related to changes in ANA over this frequency range. Above 0.3 Hz, the coherence was low, suggesting that RNA unrelated to ANA existed in the frequency range. In animals without AP perturbations, power spectrum of RNA resided over 0.2-5 Hz with a broad peak at 1 Hz, which may represent central activity. Our results suggest that over 0.02-0.3 Hz the relationship between arterial baroreceptor afferent nerve activity and RNA is linear and instantaneous but above 0.3 Hz it is not linear possibly due to an interaction between central activity and arterial baroreflex.