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PubMed1990

Selective dysfunction of the vagal component of the baroreflex following cerebral ischemia: protection by ifenprodil and flunarizine.

Baroreflex sensitivity assessed from the phenylephrine-induced reflex bradycardia was significantly decreased following 5 min global incomplete cerebral ischemia in pentobarbitalized dogs. Although bilateral vagotomy in the cervical region decreased baroreflex sensitivity by about 50% in sham-operated animals, it hardly affected the baroreflex in animals subjected to ischemia. The extent of the decrease in the influence of vagotomy on the baroreflex was dependent on the severity of ischemia in the dorsal medulla oblongata. In animals vagotomized before ischemia, no significant decrease in baroreflex sensitivity was observed following ischemia. Pretreatment with ifenprodil or flunarizine, 1 mg/kg i.v., 5 min prior to ischemia prevented the post-ischemic decrease in baroreflex sensitivity. Vagotomy decreased baroreflex sensitivity during the reperfusion period in these treated animals. These results suggest that the post-ischemic attenuation of reflex bradycardia may be due to a selective dysfunction of the vagal component of baroreflex, which can be prevented by the cerebroprotective agents.

Animals↗
PubMed1989

Comparison of baroreflex sensitivity and heart period variability after myocardial infarction.

In animals, baroreflex sensitivity is inversely related to the likelihood of ventricular fibrillation during myocardial ischemia. After myocardial infarction in human patients, reduced baroreflex sensitivity is associated with increased mortality. A reduced standard deviation of normal RR intervals over a 24 h period is also associated with reduced survival after myocardial infarction. Therefore, 32 normotensive men who had survived their first myocardial infarction were studied to define the relation between baroreflex sensitivity assessed with phenylephrine injection and three Holter electrocardiographic measures of tonic vagal activity: the percent of successive normal RR intervals greater than 50 ms, the root mean square successive difference of normal RR intervals and the power in the high frequency energy of the normal RR interval power spectrum. Correlations among the Holter measures of heart period variability were greater than or equal to 0.94, indicating that these measures are so strongly correlated that any one of them can be used to represent the others. Baroreflex sensitivity showed weaker correlations with the three Holter variables (0.57 to 0.63), indicating that the Holter measures did not accurately predict baroreflex sensitivity. Baroreflex sensitivity showed a stronger correlation with the three Holter variables during the night than during the day. Baroreflex sensitivity and tonic vagal activity reflected by Holter variables were reduced more in patients with inferior myocardial infarction than in those with anterior infarction. The relative utility of baroreflex sensitivity and Holter measures of tonic vagal activity in predicting sudden cardiac death after myocardial infarction needs to be evaluated in a large prospective study.

Circadian Rhythm↗
PubMed1992

Effects of converting enzyme inhibition on baroreflex sensitivity in patients with myocardial infarction.

BACKGROUND: Baroreflex sensitivity provides useful prognostic information in patients after acute myocardial infarction. However, no data are available about the effects of converting enzyme inhibition on this variable. OBJECTIVES: The aim of the study was to evaluate the effects of angiotensin-converting enzyme inhibition on baroreflex sensitivity in patients after uncomplicated myocardial infarction. METHODS: Twenty-five patients after uncomplicated myocardial infarction underwent baroreflex sensitivity evaluation 72 to 96 h after symptom onset and after 4 days of captopril therapy. Twenty additional patients with the same characteristics were evaluated at the same time intervals before and after placebo administration to identify spontaneous baroreflex sensitivity variations. Baroreflex sensitivity was assessed by calculating the regression line relating phenylephrine-induced increases in systolic blood pressure to the attendant changes in the RR interval. RESULTS: The mean baroreflex sensitivity value increased after captopril administration from 6.5 +/- 4.2 to 11.8 +/- 6.1 ms/mm Hg (p less than 0.01) and in individual analyses increased by greater than 2 ms/mm Hg in 68% of patients. Mean plasma renin activity increased after captopril from 3.7 +/- 2.4 to 8.5 +/- 4.9 ng/ml per h (p less than 0.005). No difference was detectable in baroreflex sensitivity and plasma renin activity values according to the site of necrosis. In the control group, baroreflex sensitivity and plasma renin activity remained unchanged between the two studies. CONCLUSIONS: This study demonstrates that in patients with uncomplicated myocardial infarction, captopril significantly improves the chronotropic response to baroreceptor stimulation.

Adult↗
PubMed1999

Orthostatic blood pressure changes and arterial baroreflex sensitivity in elderly subjects.

BACKGROUND: orthostatic hypotension in elderly people is often attributed to diminished afferent baroreflex sensitivity, but this has not been demonstrated. We examined the hypothesis that postural change in blood pressure is related to baroreflex sensitivity, independent of the confounding effect of baseline blood pressure. METHODS: we studied 25 active, untreated elderly subjects free of postural symptoms (mean age 70 +/- 1 years): 16 with hypertension (clinic blood pressure 194 +/- 6/98 + 3 mmHg) and nine normotensive controls (clinic blood pressure 134 + 3/77 + 3 mmHg). We assessed baroreflex sensitivity from the heart rate and blood pressure responses to the Valsalva manoeuvre and a pressor and depressor stimulus (bolus phenylephrine injection or sodium nitroprusside infusion respectively). Subjects were then passively tilted to 60 degrees and maximum changes in systolic blood pressure, heart rate, forearm blood flow and forearm vascular resistance recorded. RESULTS: maximum change in systolic blood pressure with head-up tilt was correlated with supine systolic blood pressure (r = 0.60, P = 0.001). Maximum change in systolic blood pressure with orthostasis was greater in the hypertensive subjects (45 +/- 4 mmHg versus 29 +/- 6, P = 0.04) and the heart rate increment was less (16 +/- 2 bpm versus 24 +/- 4, P = 0.02). The increase in forearm vascular resistance with tilt was similar in the two groups (47 +/- 11 versus 38 +/- 7 units, P = 0.52). All three methods of assessing baroreflex sensitivity showed a reduction in the hypertensive subjects (all P < or = 0.02). Lower values of baroreflex sensitivity were related to greater falls in systolic blood pressure with tilt, after adjustment for the baseline level of systolic blood pressure. CONCLUSIONS: we found a relationship between baroreflex sensitivity and the systolic blood pressure fall with orthostasis, even after adjustment for prevailing systolic blood pressure. Despite equivalent changes in forearm vascular resistance with tilt, greater falls in systolic blood pressure were seen in hypertensive subjects than in normotensive controls, due in part to an inadequate baroreflex-mediated heart rate response. The postural fall in blood pressure often observed in elderly hypertensive subjects may be related to the reduced baroreflex sensitivity seen in this condition.

Aged↗
PubMed1993

Hypotensive effect of clonidine is not mediated by enhanced baroreflex gain in rats.

We wished to examine whether enhanced depressor baroreflexes contribute to the hypotensive effect of clonidine in rats. Clonidine's hypotensive effect and clonidine's effect on baroreflex gain mean heart rate/mean blood pressure, (delta HR/delta BP) were compared under two conditions: in conscious rats with intact baroreflex control of HR, and in pentobarbital-anesthetized (PA) rats in which baroreflex control of HR is obtunded. Clonidine produced greater hypotension and bradycardia in PA rats than in conscious rats, but this greater hypotension was not associated with enhancement of baroreflex gain. Instead, clonidine-induced hypotension in PA rats was associated with a further decrease in baroreflex gain, whereas hypotension in conscious rats was not associated with any change in baroreflex gain. Selective pharmacologic blockade of sympathetic (i.e., with atenolol treatment) or parasympathetic (i.e., with methyl-atropine treatment) control of HR showed that clonidine decreased baroreflex gain in PA rats through inhibition of sympathetic control of HR. This study suggests that clonidine's hypotensive effect is not associated with enhancement of reflex bradycardic responses in rats.

Anesthesia↗
PubMed1991

Arterial baroreflex inhibition by gastric distension in rats: mediation by splanchnic afferents.

Arterial baroreflexes are known to be reset during activation of defense area and somatosensory receptors-afferents. Here we report that viscerosensory activation also inhibits the baroreflexes. In chloralose-urethan-anesthetized, succinylcholine-immobilized, and artificially ventilated rats, the aortic depressor nerve was electrically stimulated while propranolol was continuously infused to elicit baroreflex hypotension (BH) and baroreflex vagal bradycardia (BVB). Hydraulic distension of the stomach with warm 0.9% NaCl solution was found to suppress BVB and BH, with a threshold intraluminal pressure at times less than 5mmHg. The gastric distension also suppressed BH in atropinized rats, suggesting that inhibition involved not only cardiac but also vascular components of baroreflexes. Bilateral splanchnectomy largely attenuated the inhibition, whereas bilateral subdiaphragmatic vagotomy had little effect. Low- as well as high-frequency stimulation of the splanchnic nerve strongly suppressed both BVB and BH, whereas only low-frequency stimulation of the subdiaphragmatic vagus inhibited baroreflexes to a slight degree. In conclusion, gastric distension suppresses BVB and BH, and this inhibition is largely mediated by afferent fibers in the splanchnic nerve. Such baroreflex inhibition may be a general consequence of mechanoreceptor activation of any visceral hollow organs because the jejunum, esophagus, and urinary bladder were all found to suppress arterial baroreflexes when distended.

Animals↗
PubMed1993

Role of V1 receptors in the action of vasopressin on the baroreflex control of heart rate.

Arginine vasopressin (AVP) elicits a larger decrease in heart rate for a given increase in arterial pressure than do other vasoconstrictors, but there is disagreement as to whether this results from an increase in baroreflex gain or a resetting of the baroreflex to a lower blood pressure. It is also unclear which type of vasopressin receptor mediates the action of vasopressin on the baroreflex. In the present study, the effects of vasopressin, selective vasopressin V1 and V2 receptor agonists, oxytocin, and a vasopressin V1 receptor antagonist on the baroreflex control of heart rate were investigated in conscious, chronically prepared rabbits. Baroreflex curves were generated with intravenous infusions of phenylephrine and nitroprusside and analyzed using a four-parameter logistic model. Intravenous infusion of vasopressin at 5 ng.kg-1.min-1 increased mean arterial pressure by 9 mmHg and decreased heart rate by 31 beats/min. The arterial pressure at the midrange of the baroreflex curve (BP50) decreased from 75.9 +/- 4.8 to 57.6 +/- 1.7 mmHg (P < 0.01), indicating a shift of the baroreflex curve to a lower pressure, but the gain did not change significantly. The actions of vasopressin on blood pressure, heart rate, and BP50 were completely blocked by pretreatment with d(CH2)5[Tyr(Me)2]AVP, a selective V1 receptor antagonist. Infusion of [Phe2,Ile3,Orn8]AVP, a selective V1 receptor agonist, produced cardiovascular effects similar to those of vasopressin and decreased the BP50 of the baroreflex from 73.0 +/- 2.2 to 63.8 +/- 2.2 mmHg (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Comparison of phenylephrine bolus and infusion methods in baroreflex measurements.

Phenylephrine (PE) bolus and infusion methods have both been used to measure baroreflex sensitivity in humans. To determine whether the two methods produce the same values of baroreceptor sensitivity, we administered intravenous PE by both bolus injection and graded infusion methods to 17 normal subjects. Baroreflex sensitivity was determined from the slope of the linear relationship between the cardiac cycle length (R-R interval) and systolic arterial pressure. Both methods produced similar peak increases in arterial pressure and reproducible results of baroreflex sensitivity in the same subjects, but baroreflex slopes measured by the infusion method (9.9 +/- 0.7 ms/mmHg) were significantly lower than those measured by the bolus method (22.5 +/- 1.8 ms/mmHg, P less than 0.0001). Pretreatment with atropine abolished the heart rate response to PE given by both methods, whereas plasma catecholamines were affected by neither method of PE administration. Naloxone pretreatment exaggerated the pressor response to PE and increased plasma beta-endorphin response to PE infusion but had no effect on baroreflex sensitivity. Thus our results indicate that 1) activation of the baroreflex by the PE bolus and infusion methods, although reproducible, is not equivalent, 2) baroreflex-induced heart rate response to a gradual increase in pressure is less than that seen with a rapid rise, 3) in both methods, heart rate response is mediated by the vagus nerves, and 4) neither the sympathetic nervous system nor the endogenous opiate system has a significant role in mediating the baroreflex control of heart rate to a hypertensive stimulus in normal subjects.

Adult↗
PubMed2000

Sympathetic activity and baroreflex sensitivity in young women taking oral contraceptives.

BACKGROUND: We tested sympathetic and cardiovagal baroreflex sensitivity during the placebo or "low-hormone" phase (LH) and 2 to 3 weeks later during the "high-hormone" phase (HH) of oral contraceptive (OC) use in 9 women. METHODS AND RESULTS: Sympathetic baroreflex sensitivity was assessed by intravenous doses of sodium nitroprusside and phenylephrine and defined as the slope relating muscle sympathetic nerve activity (by microneurography) and diastolic blood pressure. Cardiovagal baroreflex sensitivity was defined as the slope relating R-R interval and systolic blood pressure. No difference was observed for resting muscle sympathetic nerve activity or plasma norepinephrine levels. However, sympathetic baroreflex sensitivity was greater and mean arterial pressure was higher during the LH than in the HH phase. Similarly, cardiovagal baroreflex sensitivity was greater in the LH than in the HH phase. CONCLUSIONS: Sympathetic and cardiovagal baroreflex sensitivities change during the 28-day course of OC use. Furthermore, changes in baroreflex sensitivity with OC differ from changes in baroreflex sensitivity during the normal menstrual cycle.

Adult↗
PubMed1995

Spontaneous cardiac baroreflex in humans. Comparison with drug-induced responses.

We compared two methods of assessment of baroreflex sensitivity in eight supine healthy volunteers during repeated baseline measurements and various conditions of cardiac autonomic blockade. The spontaneous baroreflex method involved computer scanning of recordings of continuous finger arterial pressure and electrocardiogram to locate sequences of three or more beats in which pressure spontaneously increased or decreased, with parallel changes in pulse intervals. The mean regression slope of all these sequences during each study condition was considered to represent the mean spontaneous baroreflex slope. In the drug-induced method, sigmoidal curves were constructed from data obtained by bolus injections of phenylephrine and nitroprusside; the tangents taken at the resting pressure of each of these curves were compared with the mean spontaneous baroreflex slopes. The two methods yielded slopes that were highly correlated (r = .96, P < .001), with significant but similar intraindividual baseline variability. Atropine virtually eliminated the baroreflex slope; subsequent addition of propranolol did not alter it further. Propranolol or clonidine alone increased average baroreflex slope to the extent that they increased resting pulse interval (r = .69 to .83). The spontaneous baroreflex method provides a reliable, noninvasive assessment of human vagal cardiac baroreflex sensitivity within its physiological operating range.

Adult↗
PubMed2000

Differential change in cardiac baroreflex sensitivity estimated by sequence and spectral analysis during etomidate anesthesia.

Spontaneous baroreflex sensitivity, high-frequency gain, (0.15-0.35 Hz), and mid-frequency gain (0.07-0.14 Hz) are noninvasive measures of cardiac baroreflex function derived by spontaneous sequence and cross-spectral analysis. To demonstrate the difference between these baroreflex estimates, 14 patients received etomidate (0.3 mg/kg bolus and 0.9 mg/kg/h infusion), lidocaine (60 mg), and vecuronium (0.1 mg/kg) by intravenous injection. The authors found that spontaneous baroreflex sensitivity and high-frequency gain were decreased (p <0.05) after etomidate anesthesia, whereas mid-frequency gain was maintained. Spontaneous baroreflex sensitivity, high-frequency gain, and mid-frequency gain, although compared simultaneously, did not change in a parallel manner. In another 5 patients, who received normal saline only, measures were unchanged. The authors conclude that spontaneous baroreflex sensitivity, high-frequency gain, and mid-frequency gain are not interchangeable. Experimental results on baroreflex control depend on the parameter selected.

Adult↗
PubMed1998

Effects of a new angiotensin-converting enzyme inhibitor, alacepril, on changes in neurohormonal factors and arterial baroreflex sensitivity in patients with congestive heart failure.

OBJECTIVE: Patients with heart failure have abnormal neurohormonal regulation during orthostatic stress, and abnormal arterial baroreflex function. This study investigated the effects of alacepril, a new angiotensin-converting enzyme inhibitor with sulfhydryls, on changes in neurohormonal factors during tilt and on the arterial baroreflex control of heart rate. METHODS: Plasma concentrations of noradrenaline, adrenaline, renin activity, angiotensin II, and atrial natriuretic peptide were measured at supine rest and after 30 degrees head-up tilt with measurements of central venous pressure and cardiac dimensions in seven patients with congestive heart failure (65 years, ejection fraction = 34%). Arterial baroreflex control of heart rate was assessed by phenylephrine bolus. The arterial baroreflex test was re-examined 3 h after oral alacepril (37.5 mg). The tilt and arterial baroreflex tests were repeated 12 weeks after alacepril treatment (50 mg x day(-1)). RESULTS: Heart rate, blood pressure, and neurohormonal factors did not differ before and after chronic alacepril, except for a trend toward an increase in renin activity (2.0 vs 4.9 ng x ml(-1) x h(-1)). Head-up tilt decreased central venous pressure (-2.5 mmHg) with a decrease in cardiac dimensions in the pre-alacepril phase. These changes were accompanied by increases in noradrenaline, adrenaline, and angiotensin II and a decrease in atrial natriuretic peptide. After chronic alacepril, the increase in noradrenaline during head-up tilt tended to be smaller (84 vs 30 pg x ml(-1)), with similar changes in central venous pressure (-3.4 mmHg) and cardiac dimensions. Both acute (3.6 vs 4.8 ms mmHg(-1)) and chronic (3.6 vs 6.7 ms mmHg(-1)) alacepril treatment was associated with a trend towards an increase in the arterial baroreflex control of heart rate. CONCLUSION: These results suggest that treatment with alacepril may cause a reduction of sympathetic activation during orthostatic stress and may enhance arterial baroreflex function in patients with mild to moderate heart failure.

Aged↗
PubMed1995

Baroreflex sensitivity during noxious stimulation in vasovagal reactors to blood donation.

Baroreflex sensitivity was assessed at rest and during constrictive pain in healthy males with and without a history of vasovagal reactions to blood donation. Continuous recordings of cardiac inter-beat interval and finger arterial pressure were obtained at rest and during repeated presentations of constrictive thigh-cuff stimulation. Baroreflex sensitivity (in msec/mm Hg) was computed according to the spontaneous sequence analysis method. Results indicated that vasovagal reactors exhibited significantly lower descending baroreflex sensitivity across all periods, and significantly lower ascending baroreflex sensitivity at rest. Baseline differences in ascending baroreflex sensitivity were eliminated during thigh-cuff stimulation, as vasovagal reactors exhibited increases in ascending baroreflex sensitivity while non-reactors exhibited decreases. These findings suggest that susceptibility to vasovagal reactions may be associated with individual differences in baroreflex sensitivity.

Adult↗
PubMed2004

Decreased baroreflex sensitivity in isoproterenol-treated mice with cardiac hypertrophy.

The baroreflex has been shown to be impaired in rat models of cardiac hypertrophy. In the present study, we investigated the effects of beta-adrenoceptor-induced cardiac hypertrophy on the baroreflex in mice. Male Swiss Webster mice weighing 20-25 g were treated with the beta-adrenoceptor agonist isoproterenol (IPM; 15 microg/g/day, s.c.) for 7 days or with vehicle (control, CM). After treatment, IPM (n=9) and CM (n=9) were anesthetized with ketamine + xylazine (91.0: 9.1 mg/kg, i.p.) and had their carotid artery and jugular vein cannulated to test the arterial baroreflex. The baroreflex was evaluated by measuring changes in heart rate (HR) in response to acute increases and decreases in mean arterial pressure (MAP) induced by bolus injections of phenylephrine and sodium nitroprusside (1.5-24.0 microg/kg, i.v.) in conscious animals. IPM showed an increased cardiac weight/body weight (1.18 +/- 0.03 mg/g) ratio compared to CM (0.95 +/- 0.03 mg/g, p<0.05), but similar values of resting MAP (108 +/- 4 vs. 111 +/- 2 mm Hg) and HR (606 +/- 25 vs. 629 +/- 26 bpm). Sigmoidal barocurve analysis showed that isoproterenol treatment significantly reduced the following parameters: baroreflex sensitivity (IPM: -4.26 +/- 0.19 vs. CM: -5.92 +/- 0.54 bpm/mm Hg, p<0.05), reflex bradycardia plateau (IPM: 387 +/- 26 vs. CM: 318 +/- 19 bpm, p<0.05) and HR range (IPM: 369 +/- 30 vs. CM: 442 +/- 20 bpm, p<0.05). Linear regression analysis of baroreflex function also showed a diminished reflex bradycardia (CM: -8.92 +/- 0.87 bpm/mm Hg vs. IPM: -4.94 +/- 0.52 bpm/mm Hg, p<0.05), but similar reflex tachycardia (CM: -3.88 +/- 0.45 bpm/mm Hg vs. IPM: -3.52 +/- 0.43 bpm/mm Hg). In conclusion, beta-adrenoceptor-induced cardiac hypertrophy in mice led to impaired sensitivity of the cardiac baroreflex, which could be due to a diminished vagal activity to the heart.

Animals↗
PubMed2005

Uptake blockade of endocannabinoids in the NTS modulates baroreflex-evoked sympathoinhibition.

Previous studies supporting a possible physiological role for an endogenous cannabinoid, arachidonylethanolamide (AEA, anandamide), showed a significant increase in AEA content in the nucleus tractus solitarius (NTS) after an increase in blood pressure (BP) and prolonged baroreflex inhibition of renal sympathetic nerve activity (RSNA) after exogenous AEA microinjections into the NTS. These results, along with other studies, support the hypothesis that endogenous AEA can modulate the baroreflex through cannabinoid CB(1) receptor activation within the NTS. This study was performed to characterize the physiological role of endogenously released cannabinoids (endocannabinoids) in regulating baroreflex control of RSNA through actions in the NTS. Endocannabinoid effects were assessed by measuring the RSNA baroreflex response to increased pressure after bilateral microinjections of AM404, an endocannabinoid transport inhibitor, into the NTS of adult male Sprague Dawley rats. AM404 blocks uptake of endocannabinoids and enhances the effects of any endocannabinoids released [M. Beltramo, et al., Functional role of high-affinity anandamide transport, as revealed by selective inhibition, Science 277 (5329) (1997) 1094-1097.] into the NTS. Therefore, it was hypothesized that microinjections of AM404 should exhibit effects similar to microinjections of exogenous AEA. In this study, AM404 microinjections into the NTS were found to significantly prolong baroreflex inhibition of RSNA compared to control, similar to effects of exogenous AEA. This effect is thought to result from an increased endocannabinoid presence in the NTS, leading to prolonged CB(1) receptor activation. These results indicate that endocannabinoids released in the NTS have the potential to modulate baroreflex control at this site in the central baroreflex pathway.

Animals↗
PubMed2005

alpha-Adrenergic and muscarinic cholinergic receptors are not involved in the modulation of the parasympathetic baroreflex by the medial prefrontal cortex in rats.

The medial prefrontal cortex (MPFC) is involved in cardiovascular control and baroreflex modulation. Recent studies indicated that stimulation of MPFC muscarinic receptors causes hypotensive responses whereas stimulation of alpha1- but not of alpha2-adrenoceptors causes pressor responses in unanesthetized rats. It has also been shown that the MPFC is involved in the modulation of the parasympathetic component of the baroreflex in rats. We report that bilateral injections of CoCl2 in the ventral portion of the MPFC (vMPFC) reduced the parasympathetic component of the baroreflex, thus confirming the involvement of local synapses. We further evaluated the effect of the pharmacologic block of vMPFC alpha1- or alpha2-adrenoceptors and muscarinic receptors on the vMPFC-related modulation of the parasympathetic component of the baroreflex in unanesthetized rats. Bilateral microinjections of 10 nmol of the selective alpha1-adrenoceptor antagonist WB4101 or 10 nmol of the selective alpha2-adrenoceptors antagonist RX821002 into the MPFC did not affect the baroreflex. Bilateral microinjections of 9 nmol of the muscarinic antagonist atropine also did not affect baroreflex activity. The present results indicate that although vMPFC alpha-adrenergic and muscarinic receptors are involved in cardiovascular regulation, they do not mediate the vMPFC-related modulation of the parasympathetic component of the baroreflex.

Animals↗
PubMed1997

Modulation of the cardiac baroreflex following reversible blockade of the parabrachial nucleus in the rat.

The parabrachial nucleus (PBN) has a prominent anatomical connection with the nucleus of the solitary tract as well as other central baroreflex centres which suggests a role for the PBN in the regulation of this cardiovascular reflex. This study examined the effects of a reversible, bilateral blockade of the PBN on the cardiac baroreflex. Male Sprague-Dawley rats were anesthetized with sodium butabarbitol and instrumented to monitor blood pressure and heart rate and for the intravenous administration of drugs. The cardiac baroreflex was evoked using bolus intravenous injections of phenylephrine (PE) and sodium nitroprusside (NaNp) at various doses and a graph of baroreflex sensitivity was constructed. Bilateral microinjections of the reversible anesthetic, lidocaine (5%, 300 nl), into the PBN did not significantly change baseline blood pressure or heart rate when compared to microinjections of saline (0.9%, 300 nl) into the PBN. The pressor or depressor responses evoked by bolus injections of PE or NaNp, respectively, were not significantly affected by the bilateral pretreatment of the PBN with lidocaine when compared to saline controls. However, approximately 30 min following lidocaine injection, the amplitudes of both the evoked-reflex bradycardia and reflex tachycardia were significantly increased by approximately 98%. The cardiovascular responses to various doses of PE and NaNp were graphed and baroreflex sensitivity curves were constructed. This graph showed an increased slope of the baroreflex sensitivity curve following lesions of the PBN. Reflex changes in heart rate returned to pre-lidocaine injection levels after approximately 2 h. The results of the present investigation suggest that the PBN participates in the modulation of the cardiac baroreflex which in turn suggests a role for this nucleus in the central integration of cardiovascular reflex function.

Analysis of Variance↗
PubMed1997

Angiotensin converting enzyme inhibition improves baroreflex-induced noradrenaline spillover responses in rabbits with heart failure.

Impaired baroreflex function is a characteristic feature of congestive heart failure (CHF), although the mechanism is obscure. This study examined the hypothesis that activation of the renin-angiotensin system contributes to baroreflex dysfunction in CHF. The acute effects of an angiotensin converting enzyme inhibitor, enalaprilat, on baroreflex-mediated changes in heart rate (HR), total and renal noradrenaline (NA) spillover rates were examined in conscious rabbits with doxorubicin-induced cardiomyopathic CHF. Studies were performed under resting conditions and in response to changes in mean arterial pressure (MAP) induced by sodium nitroprusside and phenylephrine infusions. Seven saline-treated (normal group) and 11 doxorubicin-treated rabbits (1 mg/kg administered intravenously twice weekly) were studied after 4 and 6 weeks' treatment. Five CHF rabbits received saline (C group) and 6 enalaprilat infusion (ACEI group) during each study period. After 4 weeks of doxorubicin, baroreflex-HR responses were normal, whereas baroreflex-NA spillover responses were enhanced. Enalaprilat infusion shifted the HR-MAP curve downwards to the left but had no effect on the NA spillover-MAP curves. After 6 weeks of doxorubicin, when CHF was established, baroreflex-HR and NA spillover curves were depressed. At this stage, enalaprilat had little effect on the HR-MAP curve but restored towards normal the NA spillover-MAP curves. The results suggest that the endogenous renin-angiotensin system contributes to attenuated baroreflex responses when CHF is established.

Adrenergic alpha-Agonists↗