Aortic Nerve Activity Research Articles

Discharges of aortic and carotid sinus baroreceptors during spontaneous motor activity and pharmacologically evoked pressor interventions.

Our laboratory has demonstrated that the cardiomotor component of aortic baroreflex is temporarily inhibited at the onset of spontaneous motor activity in decerebrate cats, without altering carotid sinus baroreflex. A reason for this dissociation may be attributed to a difference in the responses between aortic nerve activity (AoNA) and carotid sinus nerve activity (CsNA) during spontaneous motor activity. The stimulus-response curves of AoNA and CsNA against mean arterial blood pressure (MAP) were compared between the pressor interventions evoked by spontaneous motor activity and by intravenous administration of phenylephrine or norepinephrine, in which the responses in heart rate (HR) were opposite (i.e., tachycardia vs. baroreflex bradycardia), despite the identical increase in MAP of 34-40 mmHg. In parallel to the pressor response, mean AoNA and CsNA increased similarly by 78-81 and by 88 % of the baseline control, respectively, irrespective of whether the pressor response was evoked by spontaneous motor activity or by a pharmacological intervention. The slope of the stimulus-response curve of the mean AoNA became greater (P < 0.05) during spontaneous motor activity as compared to the pharmacological intervention. On the other hand, the stimulus-response curve of the mean CsNA and its slope were equal (P > 0.05) between the two pressor interventions. Furthermore, the slopes of the stimulus-response curves of both diastolic AoNA and CsNA (defined as the minimal value within a beat) exhibited a greater increase during spontaneous motor activity. All differences in the slopes of the stimulus-response curves were abolished by restraining HR at the intrinsic cardiac frequency. In conclusion, mean mass activities of both aortic and carotid sinus baroreceptors are able to encode the beat-by-beat changes in MAP not only at rest but also during spontaneous motor activity and spontaneous motor activity-related reduction of aortic baroreceptor activity is denied accordingly.

Signal transduction of aortic and carotid sinus baroreceptors is not modified by central command during spontaneous motor activity in decerebrate cats

Our laboratory has suggested that central command provides selective inhibition of the cardiomotor component of aortic baroreflex at the start of exercise, preserving carotid sinus baroreflex. It is postulated that central command may modify the signal transduction of aortic baroreceptors, so as to decrease aortic baroreceptor input to the cardiovascular centers, and, thereby, can cause the selective inhibition of aortic baroreflex. To test the hypothesis, we directly analyzed the responses in multifiber aortic nerve activity (AoNA) and carotid sinus nerve activity (CsNA) during spontaneous motor activity in decerebrate, paralyzed cats. The increases of 62-104% in mean AoNA and CsNA were found during spontaneous motor activity, in proportion to a rise of 35 ± 3 mmHg (means ± SE) in mean arterial blood pressure (MAP), and had an attenuating tendency by restraining heart rate (HR) at the lower intrinsic frequency of 154 ± 6 beats/min. Brief occlusion of the abdominal aorta was conducted before and during spontaneous motor activity to produce a mechanically evoked increase in MAP and, thereby, to examine the stimulus-response relationship of arterial baroreceptors. Although the sensitivity of the MAP-HR baroreflex curve was markedly blunted during spontaneous motor activity, the stimulus-response relationships of AoNA and CsNA were not influenced by spontaneous motor activity, irrespective of the absence or presence of the HR restraint. Thus, it is concluded that aortic and carotid sinus baroreceptors can code beat-by-beat blood pressure during spontaneous motor activity in decerebrate cats and that central command is unlikely to modulate the signal transduction of arterial baroreceptors.

Chronic inhibition of standing behaviour alters baroreceptor reflex function in rats

To investigate whether daily orthostatic stress during development is an important factor affecting arterial baroreceptor reflex function, we examined the effect of chronic inhibition of upright standing behaviour on the baroreceptor reflex function in rats. Upright standing behaviour was chronically inhibited during the developmental period between 3 and 8 weeks of age in Sprague-Dawley rats and heart rate (HR) and aortic nerve activity in response to increased and decreased mean arterial pressure (MAP) was measured after the treatment period. The baroreceptor cardiac gain in the rats grown without standing behaviour was significantly lower than the control rats grown in a normal commercial cage (1.0 +/- 0.1 beats min(-1) mmHg(-1) vs. 1.6 +/- 0.2 beats min(-1) mmHg(-1), P < 0.05). The range of HR change in the MAP-HR functional curve was also lowered by chronic inhibition of orthostatic behaviour (56.2 +/- 5.9 beats min(-1)) compared with that of the control rats (76.8 +/- 6.9 beats min(-1), P < 0.05). However the aortic afferent function remained normal after the treatment period, indicating that the attenuated baroreceptor reflex function may be due to other mechanisms involving functional alterations in the cardiovascular centres, efferents and/or peripheral organs. Body weight and adrenal weight were not affected by the inhibition of orthostatic behaviour, suggesting that the animals were not exposed to specific stress by this treatment. These results indicate that active haemodynamic changes induced by orthostatic behaviour are an important factor for setting the basal level of reflex function during development. Moreover, our experimental model may be useful for studying mechanisms of attenuated baroreceptor reflex observed after exposure to a chronic inactive condition.

Ramp rate of blood pressure changes does not affect aortic afferent sensitivity in anesthetized rats

To investigate whether the rate of change in blood pressure affects the sensitivity of the aortic baroreceptor afferent response, the change in aortic nerve activity (ANA) to two different rates of ramp increase in mean blood pressure (MBP), elicited by phenylephrine administration, was determined in the rat under urethane (1.5gkg−1) anesthesia. The sensitivity of the increase in ANA following a rapid (average ramp rate, 9.14±0.60mmHgs−1, n=11) or gradual (1.78±0.24mmHgs−1, n=11) increase in MBP was 2.03±0.14% and 1.81±0.20% of baseline mmHg−1, respectively. These values were not significantly different from each other (P=0.16). Furthermore, we found no correlation between the rate of ramp increase in MBP and the sensitivity of the increase in ANA (r=0.24, P=0.29, n=22). These results suggest that, at least within the normal physiological range of MBP, the rate of the ramp change in blood pressure does not affect aortic baroreceptor afferent sensitivity in the anesthetized rat.

Developmental changes in functional characteristics of aortic baroreceptor afferents in rats

To investigate postnatal developmental changes in functional characteristics of the afferent pathway of the aortic baroreceptor reflex, the responses of aortic nerve activity (ANA) to blood pressure (BP) changes elicited by phenylephrine and sodium nitroprusside administration were tested in 3-, 8- and 20-week-old male rats under chloralose (60 mg kg(-1) i.p.) and urethane (600 mg kg(-1) i.p.) anaesthesia. The function curve of ANA in response to BP changes showed a sigmoid shape that shifted to the right from 3 to 8 weeks of age. The maximal activity and maximal gain of the aortic nerve, which were calculated by a logistic function analysis, were significantly higher in 20-week-old rats (maximal activity, 532 +/- 47% of baseline; maximal gain, 7.9 +/- 0.8% of baseline mmHg(-1); n = 9) than in 3-week-old rats (maximal ANA, 268 +/- 25% of baseline, P < 0.001; maximal gain, 4.9 +/- 0.5% of baseline mmHg(-1), P < 0.01, n = 9) and 8-week-old rats (maximal ANA, 309 +/- 18% of baseline, P < 0.001; maximal gain, 4.9 +/- 0.3% of baseline mmHg(-1), P < 0.01, n = 11). These results suggest that the operating point of aortic baroreceptor afferents is reset to the higher pressure level during development from 3 to 8 weeks of age and, thereafter, the afferent gain increases from 8 to 20 weeks of age. This functional change may be an important factor to prevent an excess increase of BP, which would result in pathophysiological problems.

Does acute hyperglycemia alter rat aortic depressor nerve function?

Because it is not known where in the reflex arch, i.e., afference, central nervous system or efferences, hyperglycemia affects baroreflex function, the present study examined the effect of short-term (30 min) hyperglycemia on aortic depressor nerve function measured by a mean arterial pressure vs aortic depressor nerve activity curve, fitted by sigmoidal regression, or by cross-spectral analysis between mean arterial pressure and aortic depressor nerve activity. Anesthetized male Wistar rats received an intravenous bolus (0.25 mL) injection, followed by 30 min of infusion (1 mL/h) of 30% glucose (N = 14). Control groups received a bolus injection and infusion of 0.9% saline (N = 14), or 30% mannitol (N = 14). Glucose significantly increased both blood glucose and plasma osmolarity (P < 0.05). Mean arterial pressure did not change after glucose, saline or mannitol infusion. Mean arterial pressure vs nerve activity curves were identical before and 10 and 30 min after the beginning of glucose, saline or mannitol infusion. Slow (0.3 Hz) oscillations of arterial pressure were induced by controlled bleeding, and cross-spectral analysis was applied to arterial pressure and aortic nerve activity. Transfer function magnitude (aortic depressor nerve activity/mean arterial pressure ratio in the frequency domain) was calculated as an index of gain of the aortic depressor nerve. Transfer function magnitude was similar in all groups during induced or spontaneous oscillations of arterial pressure. In conclusion, the present study demonstrates, by means of two different approaches for assessing baroreceptor function, that aortic depressor nerve activity was not altered by short-term (30 min) hyperglycemia.

Effects of spaceflight on postnatal development of arterial baroreceptor reflex in rats

It has been reported that spaceflight attenuates the arterial baroreceptor reflex. As this reflex function changes dramatically during postnatal development, we hypothesized that space flight depresses the developmental changes of the reflex system. To test this hypothesis, we evaluated the baroreceptor reflex function in rats, which were exposed to a microgravity environment on a space shuttle 9-25 days after birth. Baroreceptor reflex sensitivity and the afferent sensitivity were evaluated by measuring heart rate (HR) and aortic nerve activity (ANA) changes in response to an increase in mean arterial pressure (MBP) derived by phenylephrine injection (20-50 microg kg(-1)) under urethane-anaesthesia. Baroreceptor reflex sensitivity (% change of HR/% change of MBP) was lower in the flight group (FLT: -0.19 +/- 0.04, n = 4) than either the asynchronous ground control group (AGC: -0.47 +/- 0.06, n = 6, P < 0.01) or the vivarium group (VIV: -0.41 +/- 0.07, n = 6, P < 0.05). This was similar to the differences of the afferent sensitivity (% change of ANA/% change of MBP) between FLT (2.07 +/- 0.30) and the control groups (AGC: 2.71 +/- 0.22, n.s.; VIV: 3.00 +/- 0.32, P < 0.05). At the end of 30 days of recovery under normal gravity conditions, however, there were no significant group differences in these parameters. conclusion: These results suggest that the space environment attenuates the postnatal development of the arterial baroreceptor reflex function in rats, which may be partially because of a depression of the postnatal development of the baroreceptor afferents. These functional alterations, however, recover to their normal level on re-exposure to the Earth's gravity.

Effects of microgravity elicited by parabolic flight on abdominal aortic pressure and heart rate in rats.

Abdominal aortic pressure (AAP), heart rate (HR), and aortic nerve activity (ANA) during parabolic flight were measured by using a telemetry system to clarify the acute effect of microgravity (microG) on hemodynamics in rats. While the animals were conscious, AAP increased up to 119 +/- 3 mmHg on exposure to microG compared with the value at 1 G (95 +/- 3 mmHg; P < 0.001), whereas AAP decreased immediately on exposure to microG under urethane anesthesia (microG: 72 +/- 9 mmHg vs. 1 G: 78 +/- 8 mmHg; P < 0.05). HR also increased during microG in conscious animals (microG: 349 +/- 12 beats/min vs. 1 G: 324+9 beats/min; P < 0.01), although no change was observed under anesthesia. ANA, which was measured under anesthesia, decreased in response to acute microG exposure (microG: 33 +/- 7 counts/s vs. 1 G: 49 +/- 5 counts/s; P < 0.01). These results suggest that microG essentially induces a decrease of arterial pressure; however, emotional stress and body movements affect the responses of arterial pressure and HR during exposure to acute microG.

Effects of the head-down tilt posture on postnatal development of the aortic baroreflex in the rabbit.

To clarify the effects of the head-down tilt (HDT) posture on the postnatal development of the aortic baroreflex, we raised rabbits from 3-4 weeks of age for 34-36 d in this posture, which simulates the headward shift of body fluid in space, and examined the structural and functional characteristics of the aortic nerves and baroreflex responses. The rabbits were divided into 3 different groups: 20 degrees HDT, environmental control (EC), and vivarium control (VIV). Left aortic nerve activity (ANA) at basal arterial pressure was defined as 100%, and the maximum ANA at maximal increase in arterial pressure was 265+/-103% (mean+/-SD, n=5) in the HDT, 482+/-170% (n=4) in the EC, and 677+/-491% (n=4) in the VIV groups. The minimum ANA at maximal decrease in arterial pressure was 67.3+/-13.8% in the HDT, 40.1+/-10.2% in the EC, and 38.6+/-13.8% in the VIV groups. The maximal change of ANA in response to maximal change in arterial pressure in the HDT group was significantly less than that of either the EC or VIV group (p<0.05). The average baroreflex gain in the HDT group was significantly less than in the VIV group (p<0.05). The number of unmyelinated fibers in the left aortic nerve in the HDT group was significantly less than that of each control group (p<0.05). Thus the development of the aortic baroreflex system is apparently depressed by the HDT posture, suggesting that similar consequences will be observed in mammals that develop in space.

Afferent baroreceptor discharge in pregnant rats.

The baroreflex function curve is shifted to lower operating pressures, efferent sympathoexcitatory responses are attenuated, and sympathoinhibitory responses are potentiated in pregnant compared with virgin rats. It has been proposed that during pregnancy, elevated levels of 3 alpha-hydroxy-dihydroprogesterone (3 alpha-OH-DHP), a major metabolite of progesterone, may contribute to this difference, because acute intravenous administration of 3 alpha-OH-DHP to virgin female rats mimics the effects of pregnancy on the baroreflex. To determine whether changes in the afferent limb might contribute to these baroreflex responses, the effects of pregnancy and 3 alpha-OH-DHP on aortic depressor nerve activity were assessed in the current study. Baroreceptor discharge curves were obtained in Inactin-anesthetized rats by recording aortic nerve activity during ramp increases and decreases in mean arterial pressure (MAP) [intravenous phenylephrine and nitroprusside infusion] before [(control, C) 15 min (E1), and 30 min (E2) after 3 alpha-OH-DHP (220 microg/kg bolus + 22 microg x kg(-1) x min(-1) infusion iv)]. Baseline blood pressure was significantly lower in pregnant (109 +/- 4.4 mmHg) compared with virgin (122 +/- 2.8 mmHg) rats. The only significant difference in the baroreceptor discharge curves was a decrease in curve midpoint in pregnant rats (virgin = 140 +/- 2.7 vs. pregnant = 124 +/- 3.6 mmHg). 3 alpha-OH-DHP had no effect on afferent baroreceptor discharge curves in either virgin or pregnant groups. These results suggest that pressure-dependent baroreceptor resetting may contribute to a shift in the baroreflex curve to lower operating pressures, but cannot completely explain differences in baroreflex function between virgin and pregnant animals.

Acute response of aortic nerve activity to free drop-induced microgravity in anesthetized rats

To test the hypothesis that arterial baroreflex was stimulated during microgravity (μG), arterial pressure (AP), intrathoracic pressure (ITP), and aortic nerve activity (ANA) were measured in anesthetized rats during 4.5 s of μG produced by free drop. A smooth and immediate reduction in G occurred during free drop, μG being achieved 100 ms after the start of the drop. Acute μG elicited an immediate and striking, but transient, increase in ANA, with no significant change in the AP, but a significant decrease in the end-expiratory ITP. The calculated transmural pressure of the aorta increased by 6.9 mmHg 2 s after the start of the drop. The increase in ANA lasted 2 s, then ANA returned to the control level, despite the calculated end-expiratory transmural pressure still being high. These results suggest that μG conditions stimulate the aortic baroreceptor by increasing transmural pressure by reducing the ITP. However, this effect is only transient, probably due to the high-pass property of the baroreceptors.

Chronic AT1 receptor blockade alters aortic nerve activity in hypertension.

In the chronic phase of coarctation hypertension (CH) we have shown both reduction in baroreceptor sensitivity (Hypertension. 1992;19[suppl II]:II-198-II-201.) and normalization of the depressed baroreceptor reflex control of heart rate, even with the persistence of hypertension in losartan-treated animals (Am J Physiol. 1995;269:H812-H818). In the present study we analyzed the effects of angiotensin II blockade on afferent aortic nerve activity of CH and sham-operated groups treated chronically with vehicle or losartan (10 mg/kg per day p.o.). CH was induced by subdiaphragmatic aortic coarctation, and the treatments lasted 8 days (4 control and 4 experimental days). Aortic pressure (conscious rats) and aortic nerve activity simultaneous to pressure (anesthetized rats) were recorded on the fourth day of the experimental period. Losartan-treated rats showed reduced tail pressure (104+/-3 versus 117+/-3 mm Hg in the vehicle group). In both groups, aortic coarctation caused a significant increase in pressure (25% and 28%, respectively) and a depression of the aortic nerve activity/pressure relationship when compared with sham-operated coarcted animals. In the physiological range of pressure changes, the depression was significantly smaller after losartan treatment (3.30+/-0.33 versus 2.18+/-0.37%/mm Hg in the losartan- and vehicle-treated CH groups, respectively, versus 5.05+/-0.33%/mm Hg in the sham-operated vehicle-treated group). Angiotensin type 1 (AT1) receptor blockade was also accompanied by reduced variability of the afferent discharge. The data suggested that apart from its pressure effect, angiotensin II acts at AT1 receptors to decrease the sensitivity of aortic afferents during physiological (+/-10 mm Hg) increases and decreases in pressure. Thus, angiotensin II may contribute to reductions of baroreceptor gain in chronic hypertension.

The effects of sevoflurane, enflurane, and isoflurane on baroreceptor-sympathetic reflex in rabbits.

This study was designed to determine the effects of sevoflurane, enflurane, and isoflurane ranging from 0.5 to 1.25 minimum alveolar anesthetic concentration (MAC) on spontaneous efferent renal sympathetic nerve activity (RNA) and the barorecptor-sympathetic reflex in rabbits. Enflurane produced significant decreases in spontaneous RNA by 22.5% +/- 6.6% at 1.0 MAC, while sevoflurane and isoflurane, at the equivalent MAC, did not. All of the anesthetics attenuated the baroreflex gain similarly when mean blood pressure (MBP) was changed by sodium nitroprusside or phenylephrine intravenously. However, the sensitivity of baroreceptors at the aortic wall was not changed by any anesthetic, because no changes in the relationship between aortic nerve activity and MBP were obtained in anesthetic concentration even at 1.25 MAC. Furthermore, these anesthetics suppressed the sympathoinhibitory response to aortic nerve stimulation above 1.0 MAC. In conclusion, enflurane inhibits RNA to a greater degree than sevoflurane or isoflurane. However, all three anesthetics depress the reflex regulation of RNA to the same degree. The suppression on the baroreceptor-sympathetic reflex does not appear to be related to a change in the receptor sensitivity on the aorta, but is mediated by suppression of the central or peripheral sympathetic integrating system.

The Effects of Sevoflurane, Enflurane, and Isoflurane on Baroreceptor-Sympathetic Reflex in Rabbits

This study was designed to determine the effects of sevoflurane, enflurane, and isoflurane ranging from 0.5 to 1.25 minimum alveolar anesthetic concentration (MAC) on spontaneous efferent renal sympathetic nerve activity (RNA) and the baroreceptor-sympathetic reflex in rabbits. Enflurane produced significant decreases in spontaneous RNA by 22.5% +/- 6.6% at 1.0 MAC, while sevoflurane and isoflurane, at the equivalent MAC, did not. All of the anesthetics attenuated the baroreflex gain similarly when mean blood pressure (MBP) was changed by sodium nitroprusside or phenylephrine intravenously. However, the sensitivity of baroreceptors at the aortic wall was not changed by any anesthetic, because no changes in the relationship between aortic nerve activity and MBP were obtained in anesthetic concentration even at 1.25 MAC. Furthermore, these anesthetics suppressed the sympathoinhibitory response to aortic nerve stimulation above 1.0 MAC. In conclusion, enflurane inhibits RNA to a greater degree than sevoflurane or isoflurane. However, all three anesthetics depress the reflex regulation of RNA to the same degree. The suppression on the baroreceptor-sympathetic reflex does not appear to be related to a change in the receptor sensitivity on the aorta, but is mediated by suppression of the central or peripheral sympathetic integrating system. (Anesth Analg 1996;82:342-8)

Role of nitric oxide in regulation of baroreceptor reflex

The possible role of nitric oxide (NO) on modulating sympathetic nerve activity through its action on baroreceptor reflex arc was investigated. l-Arginine, a precursor of NO, and N G - monomethyl- l-arginine ( l-NMMA) , an inhibitor of NO synthase, were separately infused intravenously in increasing doses in 126 pentobarbital-anesthetized rabbits. Mean arterial pressure (MAP), heart rate (HR), aortic nerve activity (ANA), cervical (CSNA) and renal sympathetic nerve activities (RSNA) were recorded. l-Arginine infusion decreased MAP ( P < 0.05), ANA ( P < 0.05), CSNA ( P < 0.05) and RSNA ( P < 0.05) without changes in HR. Infusion of d-arginine, an enantiomer of l-arginine, and simultaneous infusion of l-arginine and l-NMMA, did not elicit such changes. l-NMMA infusion increased MAP ( P < 0.05) and ANA ( P < 0.05) and decreased HR ( P < 0.05), while it tended to increase CSNA and RSNA without significance. Infusion of l-arginine or l-NMMA did not alter the slope of ANA, CSNA, RSNA, or HR in relation to MAP. These results suggest that NO modulates efferent sympathetic nerve activity, not by altering the afferent or efferent limbs of the baroreceptor reflex arc, but by interacting with the sympathetic pathway in the central nervous system.

Blockers of the L-arginine-nitric oxide-cyclic GMP pathway facilitate baroreceptor resetting.

We investigated the role of nitric oxide on rapid (25- and 40-minute) baroreceptor resetting during the onset of acute hypertension in rats treated with NG-nitro-L-arginine, an inhibitor of nitric oxide synthesis, and methylene blue, an inhibitor of guanylate cyclase. The effect of treatment with glibenclamide, an ATP-dependent K+ channel blocker, was also investigated. Arterial hypertension was provoked in a ramp progression by the drug NG-nitro-L-arginine alone or in association with aortic coarctation. Whole aortic nerve activity and carotid pressure were recorded in the anesthetized rats. The extent of rapid resetting was evaluated by means of the ratio (delta Systolic Threshold Pressure/delta Control Diastolic Pressure) x 100 as well as by the extent of displacement of the pressure-nerve activity curve defined by the ratio (delta Mean Arterial Pressure at 50% of maximum activity/delta Mean Arterial Pressure) x 100. All groups gave the same increase in mean arterial pressure at 25 and 40 minutes after the onset of hypertension. A greater extent of resetting to hypertensive levels was observed in the treated groups compared with coarctation alone. At 40 minutes after the onset of hypertension, the coarctation and nitro-L-arginine groups exhibited a further increase in the extent of resetting. The rats submitted to glibenclamide plus coarctation presented a slight but significant decrease in gain. These findings suggest that an active L-arginine-nitric oxide-cyclic GMP pathway blunts rapid resetting during the onset of hypertension. In addition, they also indicate that ATP-dependent K+ channels can also modulate rapid resetting of the baroreceptors to hypertensive levels.

Effects of CGRP on baroreflex control of heart rate and renal sympathetic nerve activity in rabbits.

We examined the effects of intravenous infusion of calcitonin gene-related peptide (CGRP) and sodium nitroprusside (SNP) on baroreceptor afferent nerve activity, renal sympathetic efferent nerve activity (RSNA), and heart rate in alpha-chloralose-anesthetized rabbits. Baroreceptor afferent nerve activity was measured from aortic nerves during CGRP- and SNP-induced hypotension. Decreases in aortic nerve activity in response to decreases in mean arterial pressure were not different during CGRP and SNP infusion. Progressive infusion of CGRP (12-120 pmol.kg-1.min-1) increased RNSA by 83 +/- 14 (mean +/- SE), 175 +/- 26, 246 +/- 36, and 343 +/- 41%, and heart rate by 8 +/- 2, 24 +/- 3, 37 +/- 4, and 47 +/- 6 beats/min during falls of blood pressure of 5, 10, 15, and 20 mmHg, respectively. These increases in RSNA and heart rate produced by CGRP were significantly greater than those produced by SNP. The alterations in heart rate and RSNA with CGRP were reversed by restoring blood pressure with phenylephrine HCl. In rabbits with sinoaortic and vagal deafferentation, the responses of heart rate and RSNA to a fall of blood pressure were abolished during both CGRP and SNP infusion. Therefore, it is suggested that the facilitated responses of heart rate and RSNA during CGRP infusion occurred by way of the arterial baroreflex arc.

Mechanisms involved in aortic baroreceptor excitation during drug-induced aortic pressure elevation in intact rabbits

Aortic baroreceptor activity during drug-induced elevation of arterial pressure in intact animals is determined not only by the magnitudes of arterial pressure elevation but also by other mechanisms such as the direct effects of drugs on aortic wall property and on baroreceptors per se. This study aimed to determine the relative contribution of arterial pressure elevation and other mechanisms on aortic baroreceptor activity during intravenous infusion of norepinephrine (NE), phenylephrine (PE) or angiotensin II (Ang II) in intact anesthetized rabbits, all of which were used to assess arterial baroreflex function in vivo. We simultaneously recorded aortic pressure (AP), afferent aortic nerve activity (ANA) and the aortic diameter (AD) during elevation of AP induced by intra-aortic balloon inflation or intravenous infusions of NE, PE, and Ang II. During Ang II-infusion or balloon inflation, AD progressively increased with increases in AP. The relationships among changes in AP, ANA, and AD were similar during balloon inflation and during Ang II infusion which indicated that increases in ANA during Ang II infusion were caused by increases in AD or strain of baroreceptors. In contrast, during NE or PE infusion, ANA increased with no changes or decreases in AD, respectively. The latter results suggest that in intact rabbits increases in ANA during NE or PE infusion resulted from mechanisms other than an increase in strain of baroreceptors, such as the direct excitatory effect on baroreceptors. Thus, different mechanisms were involved in aortic baroreceptor excitation in intact rabbits during elevation of AP caused by the vasopressor drugs, which are commonly used to assess arterial baroreflex function in vivo.

Effects of systemic ethanol on medullary vasomotor neurons and baroreflexes

The acute effects of systemic ethanol on reticulospinal sympathoexcitatory neurons were examined in vivo in anesthetized, paralyzed rats. Ethanol (0.45 g/kg, i.v.) potentiated the depressant effect of locally applied γ-aminobutyric acid (GABA) but attenuated the excitatory effect of l-glutamate. The baroreflex-mediated inhibition of these neurons and sympathetic nerve activity were partially depressed by the agent while aortic nerve activity and its sensitivity to changes in arterial pressure were not altered. These results suggest that systemic ethanol may markedly influence cardiovascular function by interfering in medullary GABAergic and glutamatergic transmissions involved in central control of the cardiovascular system.

Exogenous prostacyclin does not sensitize arterial baroreceptors

It has been shown that prostacyclin (PGI2) sensitizes cardiac receptors. However, the effects of PGI2 on arterial baroreceptors are not well understood. In rabbits anesthetized with alpha-chloralose (n = 12), we examined reflex changes in multiunit efferent renal sympathetic nerve activity (RSNA) during hypotension caused by intravenous PGI2 (0.1, 0.2, 0.5, 1.0, 2.0 micrograms/kg), nitroglycerin (NG; 5, 10, 20, 50, 100 micrograms/kg), and sodium nitroprusside (SNP; 5, 10, 20, 50, 100 micrograms/kg) before and after bilateral vagotomy. Before vagotomy, RSNA increased during hypotension caused by NG or SNP (P less than 0.01) but did not significantly change during comparable hypotension caused by PGI2. After vagotomy, PGI2 increased RSNA as much as NG or SNP. In another group (n = 6), we examined the changes in aortic pressure (AoP), multiunit afferent aortic nerve activity (ANA), and the aortic diameter (AoD) during hypotension caused by intravenous PGI2, NG, and SNP. The relationship between changes in AoP and those in ANA did not differ during hypotension caused by the three drugs. The relationship between changes in AoP and those in AoD and that between changes in AoD and those in ANA also did not differ. Finally, we examined changes in AoP, ANA, and AoD during ramp increases or decreases of AoP caused by intravenous angiotensin II or NG under background infusion of saline, PGI2, or SNP (n = 6). The relationship among these variables did not differ during infusion of PGI2 and SNP. These results suggest that PGI2 stimulates cardiac receptors with vagal afferents but does not sensitize arterial baroreceptors.