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PubMed1989

A central mechanism of acute baroreflex resetting in the conscious dog.

The role of the central nervous system in the mechanism(s) involved in acute carotid baroreflex resetting was studied in six conscious, chronically instrumented, aortic-denervated dogs. Dogs were prepared for reversible vascular isolation of the carotid sinuses. Acute baroreflex resetting was induced by holding the left carotid sinus pressure (LCcsp) at a given value for 20 minutes using a pulsatile pressure control system while at the same time keeping the right carotid sinus pressure (RCSP) at a subthreshold level (approximately 40 mm Hg). At the end of the 20 minutes, the LCcsp) was reduced to approximately 20 mm Hg, and a baroreflex (RCSP-mean arterial pressure [MAP]) curve was generated on the right carotid sinus using static-step increases in carotid sinus pressure. At the control LCcsp of 100 mm Hg, the RCSP-MAP baroreflex had a threshold pressure (Pth) of 86.6 +/- 3.1 mm Hg and a set point pressure (Psp) of 104.7 +/- 2.5 mm Hg. Increasing LCcsp) to 140 mm Hg for 20 minutes caused these parameters for the right carotid baroreflex to increase. Pth and Psp increased by 18.4 +/- 4.0 and 14.2 +/- 3.0 mm Hg, respectively (p less than 0.05). The baroreflex curve, therefore, was shifted upward and to the right. Decreasing LCcsp to 60 mm Hg caused Pth and Psp to decrease by 24.7 +/- 5.0 and 18.1 +/- 2 mm Hg, respectively (p less than 0.05). The baroreflex curve was therefore shift downward and to the left. The percent of resetting of Pth and Psp was 46 +/- 9% and 36 +/- 8%, respectively, when LCcsp was 140 mm Hg.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Baroreflex control of renal sympathetic nerve activity is preserved in heart failure despite reduced arterial baroreceptor sensitivity.

The purpose of this study was to determine if arterial baroreflex control of sympathetic nerve traffic is impaired in heart failure. We recorded renal nerve activity during changes in arterial pressure while simultaneously recording from aortic baroreceptor afferent fibers in 10 dogs with heart failure induced by rapid ventricular pacing and in 10 sham animals. Sensitivity of the aortic baroreceptors (percent change in nerve activity per millimeters mercury change in mean arterial pressure) was reduced in the heart failure group (heart failure, 2.3 +/- 0.3; sham, 3.6 +/- 0.4, p = 0.02). Despite the reduced sensitivity of aortic baroreceptors in heart failure, there was no difference in the baroreflex gain of renal nerve activity (heart failure, -5.5 +/- 1.4; sham, -5.8 +/- 1.3, p = NS). These values tended to decrease in both groups after vagotomy. The relation between baroreceptor input and renal sympathetic output, or central baroreflex gain (percent change in renal nerve activity divided by percent change in aortic nerve activity) was similar in both groups before vagotomy (heart failure, -2.4 +/- 0.6; sham, -2.3 +/- 0.5, p = NS). Vagotomy reduced central gain in the sham group (-0.9 +/- 0.1, p = 0.03) but not in the heart failure group (-1.7 +/- 0.5, p = NS), suggesting that the contribution of vagal afferents in the baroreflex arc is reduced in heart failure. Baroreflex control of R-R interval was attenuated in heart failure when assessed by blood pressure elevation but not reduction, indicating abnormal parasympathetic but preserved cardiac sympathetic mechanisms in heart failure. Thus, dogs with heart failure exhibit reduced sensitivity of aortic baroreceptors but preserved baroreflex control of renal nerve activity. Reduced baroreceptor sensitivity with preservation of baroreflex control of sympathetic nerve activity may contribute to the sympathoexcitatory state known to exist in heart failure.

Afferent Pathways↗
PubMed1990

Baroreflex control of renal sympathetic nerve activity is potentiated at early phase of two-kidney, one-clip Goldblatt hypertension in conscious rabbits.

Conscious normotensive and two-kidney, one-clip Goldblatt hypertensive rabbits were studied to determine the sensitivity of the arterial baroreflex control of renal sympathetic nerve activity (RSNA) and heart rate. The relations of the mean arterial pressure-RSNA and mean arterial pressure-heart rate were examined over a wide range of blood pressures produced by infusions of phenylephrine and nitroglycerin. The maximum slope obtained by logistic function analysis was considered to represent the baroreflex sensitivity. In the early hypertensive group (n = 8; mean arterial pressure +/- SEM, 88 +/- 2 mm Hg) on day 5 after renal clip application, the maximum slope of the mean arterial pressure-RSNA relation was -11.3 +/- 1.2, which was significantly greater than that of the sham normotensive group (-6.9 +/- 0.3, p less than 0.05). The maximum slope (-4.3 +/- 0.2) of the mean arterial pressure-RSNA relation in the late hypertensive group (n = 8; mean arterial pressure, 96 +/- 3 mm Hg) on day 21 after renal clipping was significantly smaller than that of another sham group (-7.2 +/- 0.2, p less than 0.05). In contrast to these changes in the baroreflex control of RSNA, the control of heart rate was attenuated according to the magnitude of mean arterial pressure. To elucidate the mechanisms underlying the potentiated baroreflex, the effects of endogenous neuropeptides were investigated. First, plasma concentrations of angiotensin II and arginine vasopressin that are known to affect the baroreflex were determined. Plasma concentrations of vasopressin (3.1 +/- 0.6 pg/ml) as well as of angiotensin II (34 +/- 7 pg/ml) were increased in the early hypertensive group, and the plasma vasopressin returned to a similar level to the sham group in the late hypertensive group (1.3 +/- 0.4 pg/ml). Second, to study endogenous effects of these neuropeptides on the baroreflex, the maximum slopes of the baroreflex curves during infusions of antagonists for the peptides were determined in the early hypertensive group. The maximum slope of mean arterial pressure-RSNA during intravertebral arterial [Sar1, Ala8]-angiotensin II (-16.4 +/- 1.5) was significantly greater (p less than 0.05), whereas the maximum slope during intravertebral arterial infusion of d(CH2)5Tyr(Me)arginine vasopressin (-4.7 +/- 0.5) was significantly smaller (p less than 0.05) than that during vehicle infusion (-11.3 +/- 1.2).(ABSTRACT TRUNCATED AT 400 WORDS)

Angiotensin II↗
PubMed1985

Interaction of cardiopulmonary and carotid baroreflex control of vascular resistance in humans.

Previous studies in experimental animals indicate an important inhibitory interaction between cardiopulmonary and arterial baroreflexes. In the dog, for example, cardiopulmonary vagal afferents modulate carotid baroreflex control of vascular resistance. On the other hand, previous studies in human subjects have not produced convincing evidence of a specific interaction between these baroreceptor reflexes. The purpose of this study was to determine whether unloading of cardiopulmonary baroreceptors in humans with nonhypotensive lower body negative pressure selectively augments the reflex vasoconstrictor responses to simulated carotid hypotension produced by neck pressure. In nine healthy subjects, we measured forearm vascular responses with plethysmography during lower body negative pressure alone (cardiopulmonary baroreflex), during neck pressure alone (carotid baroreflex), and during concomitant lower body negative pressure and neck pressure (baroreflex interaction). Lower body negative pressure produced a greater than twofold augmentation of the forearm vasoconstrictor response to neck pressure. This increase in resistance was significantly greater (P less than 0.05) than the algebraic sum of the increase in resistance from lower body negative pressure alone plus that from neck pressure alone. In contrast, lower body negative pressure did not potentiate the forearm vasoconstrictor responses either to intra-arterial norepinephrine or to the cold pressor test. Thus, the potentiation of the vasoconstrictor response to neck pressure by lower body negative pressure cannot be explained by augmented reactivity to the neurotransmitter or to a nonspecific augmentation of responses to all reflex vasoconstrictor stimuli. In conclusion, nonhypotensive lower body negative pressure selectively augments carotid baroreflex control of forearm vascular resistance. These experiments demonstrate a specific inhibitory cardiopulmonary-carotid baroreflex interaction in humans.

Adolescent↗
PubMed1985

Relative contribution of aortic and carotid baroreflexes to heart rate control in man during steady state and dynamic increases in arterial pressure.

We studied the contribution of carotid vs. extracarotid baroreceptors in control of heart rate in normal humans. We measured heart interval (HI) and arterial pressure during steady-state infusion of phenylephrine (PE). PE increased mean arterial pressure (MAP) by 13 +/- 2 mmHg (mean +/- SEM; n = 10) and thus stimulated both carotid and aortic baroreceptors. Neck pressure (NP) was applied during PE infusion to counter the increase in transmural carotid sinus pressure, thus leaving only aortic baroreceptors stimulated by the increase in arterial pressure. PE infusion alone prolonged HI by 230 +/- 24 ms (P less than 0.05). Application of NP attenuated the HI response to 65 +/- 22 ms above control (P less than 0.05 vs. PE alone). During these steady-state increases in arterial pressure, elimination of the carotid baroreflex contribution reduced the HI prolongation by 41-70% in five subjects and by greater than 93% in five subjects. We also measured the HI response to dynamic ramp elevation of systolic arterial pressure (SAP) using bolus administrations of PE. Baroreflex control was calculated from the slope of the regression correlating SAP to succeeding HI for PE alone (carotid and aortic baroreceptor activation) and for PE plus superimposed dynamic NP at levels equal to the increases in SAP (aortic baroreceptor activation). During PE alone, the baroreflex slope was 20.2 +/- 2.9 ms/mmHg (n = 10). During PE plus NP, the baroreflex slope was reduced by 30% to 14.1 +/- 2.8 ms/mmHg (P less than 0.02 vs. during PE alone). Thus, during dynamic increases in arterial pressure, eliminating the carotid baroreflex contribution reduced the HI response by 30%. These studies indicate that extracarotid (presumably aortic) and carotid baroreflexes both participate in control of heart rate in humans. Extracarotid (aortic) baroreflexes appear to have the greater role in control of heart rate during dynamic increases in arterial pressure.

Adult↗
PubMed1993

Effects of fentanyl, diazepam, and the combination of both on arterial baroreflex and sympathetic nerve activity in intact and baro-denervated dogs.

The combination of fentanyl and diazepam significantly decreases systemic vascular resistance and blood pressure. We attempted to elucidate the reason the combination of these drugs can reduce blood pressure. In alpha-chloralose-anesthetized dogs, we investigated the effects of fentanyl and diazepam on mean arterial pressure (MAP) and arterial baroreflex control of renal sympathetic nerve activity (RSNA) in both intact (Study 1) and baroreflex-denervated dogs (Study 2). Study 1 included five dogs that received fentanyl 10 micrograms/kg followed by diazepam 0.4 mg/kg after a 10-min interval. Five more received both drugs in reversed sequence. The arterial baroreflex depressor test was performed with sodium nitroprusside before and after administration of each drug. Sensitivity of arterial baroreflex was examined by using the ratio of maximum increase of RSNA to maximum decrease of MAP (delta RSNA/delta MAP). RSNA and MAP significantly decreased only after both drugs had been administered (P < 0.05). Fentanyl alone did not attenuate arterial baroreflex sensitivity. Diazepam after fentanyl and diazepam alone attenuated baroreflex sensitivity to the same extent (P < 0.05). Study 2 comprised 14 dogs that underwent further surgical preparation of bilateral carotid sinus, aortic, and vagal nerve denervations. Seven received fentanyl, 5 and 10 micrograms/kg, and the other seven received diazepam, a total of 0.4 mg/kg. Fentanyl decreased both RSNA and MAP. Diazepam decreased only MAP significantly. The results indicate that fentanyl decreases mainly sympathetic outflow, whereas diazepam attenuates arterial baroreflex. We conclude that these combined effects of fentanyl and diazepam significantly decrease arterial blood pressure.

Animals↗
PubMed1981

Time-dependent changes in open-loop gains of baroreflex systems after massive hemorrhage.

To quantify the effects of massive hemorrhage (5 ml/kg body weight) on the individual arterial baroreflex systems in the dog, changes in the open-loop gains of the intact arterial pressure control system (Gintact), the carotid sinus baroreflex system (GCS), and the vagally mediated and aortic arch baroreflex systems (GV) were measured repeatedly from the response to quick mild hemorrhage (2 ml/kg body weight) before and after massive hemorrhage. Fifteen mongrel adult dogs were divided into 3 groups. i.e., the control, vago-aortic nerve-severed, and carotid sinus-denervated groups. The dogs anesthetized with Nembutal (35 mg/kg body weight) were bled by 2 ml/kg body weight within 2 sec through a catheter inserted into the abdominal aorta. The arterial pressure change after mild hemorrhage was monitored via a catheter placed in the aortic arch. The open-loop gain of the baroreflex system was assessed as (delta API/delta APS--1), where delta API and delta APS are the immediate and steady-state falls in arterial pressure following mild hemorrhage. The mean values of Gintact, GCS, and GV before massive hemorrhage were 7.8, 2.0, and 1.8, respectively. Since Gintact is not a simple summation of GCS and GV, it is speculated that the carotid sinus baroreflex system interacts in a facilitatory way with the vagally mediated and aortic arch baroreflex systems. After massive hemorrhage, Gintact changed along a time course of parabolic form, whereas GCS did not change and GV decreased. These results suggest that the time-dependent change of Gintact after massive hemorrhage depends on the change in the open-loop gain of the baroreflex system making a facilitatory interaction.

Animals↗
PubMed1986

Central opioid receptors and baroreflex control of sympathetic and cardiovascular function.

The effect of central opioid receptor activation and blockade on arterial baroreflex regulation of cardiovascular function was studied. Baroreceptor reflexes were elicited in urethane-anesthetized rats by graded electrical stimulation of the aortic nerve while mean arterial pressure, heart rate and sympathetic nerve activity were recorded simultaneously. Baroreflex response curves were constructed after intracisternal administration of saline vehicle, after intracisternal infusion of the relatively selective mu and delta opioid receptor agonists D-Ala2-MePhe4-Gly(ol)5 enkephalin (DAGO), or D-Ala2-D-Leu5 enkephalin (DADLE) respectively, and again after i.v. naloxone. Reflex reductions in mean arterial pressure, heart rate and sympathetic nerve activity elicited by aortic nerve stimulation were attenuated in a dose-related fashion by intracisternal DAGO. Opioid effects were greatest at low levels of baroreceptor activation and became progressively less marked as the frequency of aortic nerve stimulation was increased. Baroreflex impairment was reversed completely by i.v. naloxone. Centrally administered DADLE also attenuated baroreceptor reflexes, but was approximately 10- to 100-fold less potent than an equimolar amount of DAGO. The effect of DADLE was reversed by a lower dose of naloxone than was required to normalize baroreflexes after DAGO. These results suggest that the effect of DADLE on baroreflexes was mediated by activation of mu rather than delta opioid receptors. No evidence was obtained to suggest a role for endogenous opioid modulation of baroreflexes because i.v. naloxone was without effect. These results demonstrate that activation of central mu opioid receptors significantly impairs baroreflex control of sympathetic and cardiovascular function.

Animals↗
PubMed1993

[Effect of intravenous lidocaine infusion on arterial baroreflex].

The purpose of the first study was to identify the relationship between reflex sympathetic nerve activity and plasma concentration of lidocaine. Lidocaine was infused in 4 different doses: 2 mg.kg-1 bolus + 100 micrograms.kg-1 x min-1, 3 mg.kg-1 bolus + 200 micrograms.kg-1 x min-1, 6 mg.kg-1 bolus + 400 micrograms.kg-1 x min-1 and 12 mg.kg-1 bolus + 800 micrograms.kg-1 x min-1. Baroreflex depressor and pressor tests using sodium nitroprusside (5-10 micrograms.kg-1) and phenylephrine (2-4 micrograms.kg-1) were performed before and at 10 min after the start of lidocaine infusion. Plasma lidocaine concentrations determined by HPLC revealed that its steady-state levels were maintained during the baroreflex tests. Baroreflex sensitivity was preserved at clinical concentrations of lidocaine (< 5 micrograms.ml-1). However, baroreflex was significantly attenuated when plasma lidocaine concentrations were above seizure levels (> 10 micrograms.ml-1). This result indicates that hemodynamic derangement observed in the lidocaine-induced CNS toxicity is, at least in part, due to the attenuated arterial baroreflex. In the second study, the author evaluated the effect of respiratory acidosis and alkalosis on the baroreflex with or without lidocaine infusion (2 mg.kg-1 + 100 micrograms.kg-1 x min-1). Respiratory acidosis (PaCO2: 65.6 +/- 3.4) enhanced the baroreflex significantly, but lidocaine infusion abolished this acidosis-induced enhancement. The author concludes that hypercarbia should be avoided in patients receiving intravenous lidocaine infusion.

Acidosis, Respiratory↗
PubMedDate not supplied

Hemodynamic correlates of baroreflex impairment of heart rate in experimental canine heart failure.

The arterial baroreflex has been shown to be depressed in both clinical and experimental heart failure. The mechanism and significance of this depression remains controversial. Part of the change may reside in the baroreceptor as well as in the target organ. Previous studies in this laboratory have shown that there is no central depression of the baroreflex in anesthetized dogs. The present study was undertaken to determine the relationship between the change in baroreflex sensitivity (BRS) and the impairment of various hemodynamic parameters during the development of chronic heart failure in conscious dogs (n = 15). The animals were instrumented to record pressures and derivatives in the left atrium, aorta and the left ventricle. Heart failure was achieved by rapid left ventricular pacing (250 bpm) until the development of clinical signs. BRS was determined by correlating systolic arterial blood pressure and pulse interval during bolus injections of nitroglycerin and phenylephrine. Data were analyzed by correlating the changes in BRS (n = 90) with respect to changes in each parameter. No or a weak correlation was found between the changes in the baroreflex and parameters of systolic function or time of pacing. A stronger correlation was found between BRS and parameters of preload such as left ventricular enddiastolic pressure and left atrial pressure (p < 0.001). In general, the bradycardia responses were depressed less than the tachycardia responses. The correlation between BRS and left atrial or left ventricular end diastolic pressure is consistent with the view that augmented input from cardiac receptors may contribute to the depressed baroreflex function in heart failure. These data also suggest that the sympathetic limb of baroreflex control of heart rate in chronic heart failure is depressed earlier and to a greater extent then the vagal limb.

Animals↗
PubMed2000

Baroreflex sensitivity as a new marker for risk stratification.

As the arterial baroreflex importantly contributes to modulation of the autonomic influences on the heart and thereby arrhythmogenesis, baroreflex sensitivity has been used as a measure of the interaction between sympathetic and parasympathetic activities at the cardiac level. The most widely applied technique both in the experimental and clinical setting is the measurement of the heart rate slowing in response to a blood pressure rise induced by small intravenous boluses of phenylephrine. Baroreflex sensitivity is expressed as ms/mmHg and prevailing vagal reflexes are reflected by the wider R-R interval lengthening. The experimental evidence that the occurrence of ventricular fibrillation was inversely related to baroreflex sensitivity, opened the way to clinical studies. The ATRAMI (Autonomic Tone and Reflexes After Myocardial Infarction) trial has definitely demonstrated not only that a depressed baroreflex sensitivity (< 3 ms/mmHg) is a strong risk factor for cardiac death, but also that the information gained by the analysis of autonomic markers adds to the information obtained by better recognized measures of cardiovascular outcome such as left ventricular function and ventricular arrhythmias. The value of a depressed baroreflex sensitivity as a risk stratifier is meaningful in patients below age 65 in combination of a simultaneously depressed left ventricular ejection fraction. In these patients, the analysis of autonomic activity might be of value in the identification of patients who may need an implantable automatic defibrillator for primary prevention of sudden cardiac death.

Animals↗
PubMed2001

Spontaneous arterial baroreflex control of the heart rate during head-down tilt in heat-stressed humans.

The purpose of this study was to elucidate the effect of raised body temperature per se during acute heat stress on the spontaneous arterial baroreflex control of heart rate (fc) in humans. To investigate whether unloading of cardiopulmonary baroreceptors during whole-body heating would alter the arterial baroreflex control of fc, we controlled loading of the cardiopulmonary baroreceptors by head-down tilt (HDT) at angles of 5 degrees, 10 degrees, 15 degrees, and 30 degrees during heat stress produced by hot-water-perfused suits. The sensitivity of the arterial baroreceptor-cardiac reflex was calculated from the spontaneous changes in beat-to-beat arterial pressure and fc. As an index of cardiopulmonary baroreceptor loading, the left atrial diameter (LAD) was measured by echocardiography. During whole-body heating, the LAD decreased with the rising body core temperature and increased with the HDT. The decreased LAD during heating almost recovered to the normothermic control level by 10 degrees HDT. In the supine position, cardiac baroreflex sensitivity remained unchanged during heating. Arterial pressure, fc and cardiac baroreflex sensitivity were not changed by HDT ranging from 5 degrees to 30 degrees during heating. These results suggest that cardiac baroreflex sensitivity remain unchanged during graded loading of the cardiopulmonary baroreceptors in heat-stressed humans. Also, we conclude that the sensitivity of the spontaneous arterial baroreflex controlling the fc is not influenced by raised body temperature per se during acute heat stress.

Adult↗
PubMed2006

Geomagnetic field modulates artificial static magnetic field effect on arterial baroreflex and on microcirculation.

Spreading evidence suggests that geomagnetic field (GMF) modulates artificial magnetic fields biological effect and associated with increased cardiovascular morbidity. To explore the underlying physiological mechanism we studied 350 mT static magnetic field (SMF) effect on arterial baroreflex-mediated skin microcirculatory response in conjunction with actual geomagnetic activity, reflected by K and K ( p ) indices. Fourteen experiments were performed in rabbits sedated by pentobarbital infusion (5 mg/kg/h). Mean femoral artery blood pressure, heart rate, and the ear lobe skin microcirculatory blood flow, measured by microphotoelectric plethysmogram (MPPG), were simultaneously recorded before and after 40 min of NdFeB magnets local exposure to sinocarotid baroreceptors. Arterial baroreflex sensitivity (BRS) was estimated from heart rate/blood pressure response to intravenous bolus injections of nitroprusside and phenylephrine. We found a significant positive correlation between SMF-induced increase in BRS and increment in microvascular blood flow (DeltaBRS with DeltaMPPG, r=0.7, p<0.009) indicated the participation of the arterial baroreflex in the regulation of the microcirculation and its enhancement after SMF exposure. Geomagnetic disturbance, as opposed to SMF, decreased both microcirculation and BRS, and counteracted SMF-induced increment in microcirculatory blood flow (K-index with DeltaMPPG; r (s)=-0.55, p<0.041). GMF probably affected central baroreflex pathways, diminishing SMF direct stimulatory effect on sinocarotid baroreceptors and on baroreflex-mediated vasodilatatory response. The results herein may thus point to arterial baroreflex as a possible physiological mechanism for magnetic-field cardiovascular effect. It seems that geomagnetic disturbance modifies artificial magnetic fields biological effect and should be taken into consideration in the assessment of the final effect.

Animals↗
PubMed2004

Carotid baroreflex function ceases during vasovagal syncope.

Despite the arterial baroreflex control of heart rate and blood pressure, vasovagal syncope is a common cause of loss of consciousness in people exposed to stimuli that reduce the central blood volume, such as head-up tilt. Carotid baroreflex function was evaluated using a rapid pulse train of neck pressure and neck suction in three conscious volunteers who developed a vasovagal episode during head-up tilt. The maximal gain of the carotid-heart rate and carotid-blood pressure baroreflex function curves were identified as measures of carotid baroreceptor responsiveness. When presyncopal symptoms developed, one further baroreflex assessment was obtained before the subjects were returned to the supine position. The bradycardia and hypotension exhibited during pre-syncope and syncope reflected a leftward and downward relocation of both the cardiac and vasomotor stimulus response curves. In addition, during the vasovagal syncope, baroreflex control was suppressed as blood pressure remained low during neck pressure stimuli. In conclusion, arterial baroreflex function ceases during vasovagal syncope.

Adult↗
PubMed1995

Baroreflex function in streptozotocin (STZ) induced diabetic rats.

To determine whether the renal sympatho-inhibition and bradycardia in responses to acute increases in arterial pressure are altered in the diabetic state, the renal nerve discharge and heart rate were measured in streptozotocin (STZ) induced diabetic (DIA) rats. Integrated renal sympathetic nerve activity and heart rate were measured before and during an acute increase in blood pressure in anesthetized (Inactin 0.1 g/kg, i.p.) control (vehicle) and DIA rats (Sprague Dawley rats injected with STZ 65 mg/kg i.p.). Blood glucose levels were significantly elevated in the DIA group compared with the control group. Baroreflex changes in renal nerve activity and heart rate were not significantly different in the DIA rats compared with control rats at a time when the renal sympatho-inhibition in response to acute volume expansion was blunted in the diabetic rats. In addition, blocking the effect of elevated angiotensin II in diabetic rats with the converting enzyme inhibitor enalapril did not change the baroreflex function in DIA rats compared with control rats. However, administration of vasopressin failed to potentiate the baroreflex in diabetic rats as it did in normal control rats. This study demonstrates that (1) the baroreflex function is normal in STZ induced diabetic rats unlike the volume reflex during the early phase of the disease, (2) blockade of the AII system does not alter baroreflex function in diabetic rats and (3) vasopressin fails to potentiate the baroreflex in diabetic rats as it does in the euglycemic normal rats.

Analysis of Variance↗
PubMed1994

Oxytocin augments baroreflex bradycardia in conscious rats.

Previous studies have demonstrated augmentation of baroreflex-mediated bradycardia by arginine vasopressin (AVP). However, the specific receptor subtype responsible for mediating this augmentation has not been determined. In the present study, experiments were performed in conscious rats to determine the possible involvement of oxytocin receptors in this response. Infusion of oxytocin at a dose that had no effect on baseline hemodynamic values significantly augmented the bradycardic response to IV bolus doses of methoxamine. Prior treatment with selective antagonists to either oxytocin, V1 vasopressinergic or V2 vasopressinergic receptors reversed this enhancement. In a separate set of experiments, baroreflex-mediated bradycardic responses to IV bolus doses of AVP were assessed. Pretreatment with the selective oxytocin receptor antagonist reversed vasopressinergic augmentation of baroreflex sensitivity. Finally, combined vasopressinergic and oxytocinergic stimulation of the baroreflex was assessed. Treatment with both AVP and oxytocin did not augment baroreflex-mediated bradycardia greater than AVP alone. We conclude from these experiments that AVP and oxytocin both augment baroreflex sensitivity, although the receptor type(s) responsible are not clear.

Animals↗
PubMed1995

Preoptic recess ablation selectively increases baroreflex sensitivity to angiotensin II in conscious rats.

Angiotensin II (ANG II) attenuates baroreflex sensitivity through central pathways. However, the specific CNS sites where ANG II inhibits baroreflexes are not completely understood. The periventricular tissue of the anteroventral third cerebral ventricle (AV3V) mediates several responses to centrally and peripherally administered ANG II. Therefore, these studies determined the effects of bilateral electrolytic ablation of AV3V periventricular tissue on reflex-induced changes in heart rate during pressor and depressor responses evoked by IV administration of phenylephrine (PE), ANG II, and nitroprusside (NP). Animals were prepared with catheters in the femoral artery and vein 10-14 days following AV3V ablation or control (CONT) surgery. The following day, baroreflex sensitivity in the conscious animals was evaluated as the slope of the regression line relating blood pressure and heart rate during IV infusion (1 min) of three doses of PE, ANG II, and NP. Baroreflex sensitivity during PE and NP infusion were equivalent in AV3V-lesioned and CONT animals. However, animals with AV3V lesions demonstrated significantly greater baroreflex sensitivity during ANG II infusion than both PE-treated AV3V-lesioned animals and ANG II-treated CONT animals. These data suggest that the impairment of baroreflex-induced bradycardia during pressor responses evoked by ANG II is mediated by tissue located in the AV3V region.

Angiotensin II↗
PubMed1995

Blockade of L-glutamate receptors in the rostral ventrolateral medulla contributes to ethanol-evoked impairment of baroreflexes in conscious rats.

This study investigated the effect of ethanol microinjected into the rostral ventrolateral medulla on the cardiovascular responses to intrarostral ventrolateral medulla administration of the excitatory amino acids L-glutamate and N-methyl-D-aspartate (NMDA) and on baroreflex-mediated heart rate responses (baroreflex sensitivity) in conscious freely moving Sprague-Dawley rats. L-Glutamate (5 nmol) or NMDA (25, 50, and 100 pmol) microinjected into the rostral ventrolateral medulla elicited pressor and bradycardiac responses. The cardiovascular responses elicited by both L-glutamate and NMDA were significantly (p < 0.05) attenuated by intrarostral ventrolateral medulla ethanol (10 micrograms) or 2-amino-5-phosphonopentanoic (2 nmol), a selective NMDA receptor antagonist, but not by ACSF. Enhancement of the cardiovascular responses to L-glutamate by intrarostral ventrolateral medulla p-chloromercuriphenylsulfonic acid (0.1 nmol), a glutamate uptake inhibitor, was reversed by subsequent ethanol, but not ACSF, microinjection. None of the treatments influenced baseline blood pressure or heart rate. Ethanol or 2-amino-5-phosphonopentanoic acid microinjected into the rostral ventrolateral medulla significantly (p < 0.05) attenuated baroreflex sensitivity tested by phenylephrine. In contrast, p-chloromercuriphenylsulfonic acid significantly (p < 0.05) enhanced baroreflex sensitivity (-2.14 +/- 0.09 vs. -3.08 +/- 0.18); subsequent ethanol microinjection reversed this enhancement (-2.90 +/- 0.21 vs. -1.86 +/- 0.24). Equal volume of ACSF had no effect on baroreflex sensitivity of pretreated rats (-3.22 +/- 0.31 vs. -2.98 +/- 0.34). These results suggest that ethanol exerts a marked inhibitory action on glutamatergic pathways within the rostral ventrolateral medulla that act to enhance baroreflex sensitivity.(ABSTRACT TRUNCATED AT 250 WORDS)

2-Amino-5-phosphonovalerate↗