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At least 19 recordsLinked to original sources
PubMed1988

Arterial baroreflex control of sympathetic nerve activity during elevation of blood pressure in normal man: dominance of aortic baroreflexes.

Arterial baroreceptors in the carotid sinus (CBR) and aortic arch (ABR) regions exert important control over heart rate and peripheral vascular responses to changes in arterial pressure. The relative roles of these two baroreflex pathways on control of sympathetic nerve activity during sustained elevation of arterial pressure in man is unknown. We therefore studied the relative contributions of the carotid versus the aortic baroreflexes on the control of muscle sympathetic nerve activity (MSNA) during elevation of arterial pressure in normal human subjects. In eight normal men (group I), we measured MSNA (microneurography) during sustained elevation of arterial pressure produced by intravenous infusion of phenylephrine (PE) alone (combined ABR and CBR activation) versus during PE infusion with superimposed application of sustained external neck pressure (NP). NP was applied during sustained PE infusion to eliminate the increase in transmural carotid sinus pressure and thus remove CBR activation, thereby causing ABR stimulation alone. Mean arterial pressure was measured directly, central venous pressure was held constant during PE infusion, and MSNA was measured as total activity (burst frequency X amplitude) and expressed as units. Infusion of PE (ABR and CBR activation) increased mean arterial pressure from 87.2 +/- 2.8 to 94.9 +/- 2.9 mm Hg (+/- SE, p less than .001). This was accompanied by a decrease in heart rate from 65.8 +/- 3.4 to 56.1 +/- 3.3 beats/min (p less than .001) and a decrease in MSNA from 236.2 +/- 47.5 to 84.5 +/- 19.3 units (p less than .001). During infusion of PE with superimposed NP (ABR activation alone), mean arterial pressure increased further to 101.2 +/- 2.9 mm Hg (p less than .001 versus control or PE alone), and heart rate returned to control levels of 62.9 +/- 2.0 beats/min (p = NS vs control; p less than .01 PE vs PE plus NP), but MSNA remained reduced at 48.6 +/- 9.2 units (p less than .01 vs control; p = NS vs PE alone). Thus, combined activation of ABR and CBR resulted in a 65 +/- 5% attenution of MSNA, while activation of ABR alone resulted in a 73 +/- 7% attenuation of MSNA. In a separate series of experiments in seven subjects (group II) we used sustained external neck suction alone to activate the CBR (leaving the ABR either unchanged or minimally deactivated) and studied the MSNA responses to this CBR activation.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1994

Baroreflex dysfunction in diabetes mellitus. II. Site of baroreflex impairment in diabetic rabbits.

In our companion paper [T. S. McDowell, M. W. Chapleau, G. Hajduczok, and F. M. Abboud, Am. J. Physiol. 266 (Heart Circ. Physiol. 35): H235-H243, 1994] we report that baroreflex-mediated bradycardia is impaired in diabetic rabbits. The purpose of the present study was to identify the site of impairment. Diabetes was induced in rabbits by alloxan (90-100 mg/kg iv; n = 7). Alloxan-treated rabbits that remained normoglycemic (n = 8) and rabbits given saline instead of alloxan (n = 4) served as controls. Twenty-four weeks after administration of alloxan or saline, rabbits were anesthetized with alpha-chloralose. Aortic baroreceptor and renal sympathetic nerve activity (RSNA) were recorded during phenylephrine- and nitroglycerin-induced changes in arterial pressure. The slope of the baroreceptor pressure-activity relation was not significantly different in diabetic rabbits (1.3 +/- 0.3%/mmHg, n = 7) compared with either alloxan-treated (1.3 +/- 0.1%/mmHg) or saline-treated normoglycemic rabbits (1.2 +/- 0.2%/mmHg). The slope of the arterial pressure-RSNA relation was not significantly different in diabetic rabbits (-3.5 +/- 0.3%/mmHg, n = 7) compared with the alloxan-treated normoglycemic rabbits (-3.0 +/- 0.4%/mmHg, n = 8) and was greater than that in saline-treated normoglycemic rabbits (-1.9 +/- 0.3%/mmHg, n = 4; P < 0.05). The decreases in heart rate in response to electrical stimulation (10 V, 2 ms, 0.5-16 Hz) of the cut peripheral end of the right cervical vagus were similar in diabetic and alloxan-treated normoglycemic rabbits.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Baroreflexes and cardiovascular regulation in hypertension.

The primary purpose of the arterial baroreflex is to keep blood pressure close to a particular set point over a relatively short period of time. The rapid resetting of arterial baroreceptor afferents toward any sustained new level of blood pressure ensures that the reflex acts as an effective buffer of short-term blood pressure fluctuations that accompany daily life but also ensures that arterial baroreflexes play little role in setting the long-term level of blood pressure. Nevertheless, the minimization of blood pressure variability by baroreflex mechanisms is important as studies suggest that a diminished baroreflex is an independent risk factor or sudden death after myocardial infarction. In hypertensive humans and animals, the baroreflex control of heart rate is diminished. Using the steady-state method for assessment of the cardiac baroreflex in rats, we have shown that the change in baroreflex sensitivity is due to a reduction in the vagal range. Although the cardiac sympathetic component of the baroreflex is normal, the level of cardiac sympathetic activity is enhanced, particularly in young hypertensive rats. We have shown that there is a stronger inverse relationship between vagal heart rate range and levels of cardiac hypertrophy than with other variables, such as blood pressure, hypertension, or indexes of vascular hypertrophy. Treatments that reduce cardiac hypertrophy restore cardiac vagal function. Centrally acting antihypertensive agents increase the sensitivity of vagal baroreceptor heart rate reflexes, mainly through an action on central alpha 2-adrenoceptors. They also reduce cardiac sympathetic activity and diminish cardiac sympathetic baroreflexes through a non-alpha 2-adrenoceptor, possibly an imidazoline receptor mechanism. Both of these effects are beneficial in hypertension, where cardiac sympathetic function is enhanced and vagal activity is reduced. Thus, these actions would be expected to cause a desirable reduction in blood pressure variability. The effect of hypertension on baroreflex control of sympathetic vasomotor function is less clear. Studies have shown diminished, normal, and enhanced sympathetic vasomotor baroreflex control. Basal renal sympathetic drive, however, appears to be increased in human essential hypertension. Our studies in conscious rabbits have shown that rilmenidine reduces renal sympathetic baroreflex function. Rilmenidine acts principally at the level of the rostral ventrolateral medullary imidazoline receptors to markedly reduce the basal renal sympathetic nerve activity and the maximum response to transient fluctuations in blood pressure. Thus, in addition to their antihypertensive actions, centrally acting agents, such as rilmenidine, reduce cardiac and renal sympathetic baroreflex responses and increase cardiac vagal baroreflex sensitivity. This provides an ideal profile of action for the restoration of baroreflex function in addition to reversal of cardiac and vascular hypertrophy in hypertension.

Animals↗
PubMed1995

Good exercise capacity at hospital discharge predicts recovery of baroreflex sensitivity after myocardial infarction.

Myocardial infarction results in depressed baroreflex sensitivity, which has been shown to be associated with increased risk of ventricular arrhythmias and sudden death. We measured baroreflex sensitivity in 37 patients with acute myocardial infarction before hospital discharge and 3 months after the infarction to find out whether the baroreflex sensitivity recovers during that period. In addition, baroreflex sensitivity was assessed in 15 healthy controls. Baroreflex sensitivity was assessed from the regression line relating the change in R-R interval to the change in systolic blood pressure following an intravenous bolus injection of phenylephrine. There was a wide inter-individual variation in the change of baroreflex sensitivity (delta baroreflex sensitivity) in infarction patients, but the average baroreflex sensitivity showed no significant change during the 3-month follow-up (10.2 + 5.6 to 11.8 +/- 7.5 ms.mmHg-1, ns) and remained lower than the baroreflex sensitivity of the controls (16.4 +/- 9.7 ms.mmHg-1, P < 0.05). delta Baroreflex sensitivity correlated significantly with exercise capacity measured before hospital discharge. When the patients were divided into tertiles according to the delta baroreflex sensitivity (-3.3 +/- 1.5 ms.mmHg-1 in the lowest tertile, 1.0 +/- 1.0 ms.mmHg-1 in the middle tertile and 7.5 +/- 4.0 ms.mmHg-1 in the highest tertile) the exercise capacity was found to increase from the lowest to the highest tertile (exercise time 357 +/- 115 s, 418 +/- 126 s and 461 +/- 141 s, respectively; P < 0.05 lowest vs highest tertile). Patients with a low exercise tolerance (exercise time < 360 s) showed a significantly smaller delta baroreflex sensitivity than patients with a good exercise tolerance (exercise time > or = 480 s) (-0.5 +/- 4.4 vs 5.3 +/- 5.4 ms.mmHg-1, P < 0.05), respectively. delta Baroreflex sensitivity was not related to the location or type of infarction, thrombolytic therapy, presence of angina pectoris or left ventricular function at the time of discharge. In conclusion, exercise capacity assessed before hospital discharge seems to be a predictor of baroreflex sensitivity recovery in patients with a recent myocardial infarction.

Aged↗
PubMed1993

Arterial baroreflex inhibition by midbrain periaqueductal grey in anaesthetized rats.

Midbrain periaqueductal grey (PAG) provokes the defense reaction when stimulated. The present study was conducted to determine whether, and how, the PAG produces baroreflex inhibition, a feature characterizing the hypothalamic defense reaction. In chloralose-urethane anaesthetized rats, baroreflex vagal bradycardia and baroreflex hypotension were provoked by aortic depressor nerve stimulation. When the PAG was electrically stimulated baroreflex vagal bradycardia was remarkably suppressed; suppression of baroreflex hypotension was observed following bilateral vagotomy. In contrast, chemical stimulation of the PAG by D,L-homocysteic acid microinjection markedly suppressed baroreflex vagal bradycardia but only minimally suppressed baroreflex hypotension. These findings suggest that whereas overall PAG stimulation inhibits not only cardiac but also vascular components of baroreflexes, inhibition of the latter component either depends largely on activation of passing fibers or requires recruitment of a larger number of PAG cell bodies. PAG inhibition of baroreflex vagal bradycardia was not affected following spinal cord transection at C1, indicating that the inhibition was exclusively central in origin and not due to peripheral, prejunctional inhibition of vagal acetylcholine release by increased cardiac sympathetic nerve activities. The PAG inhibition of baroreflexes was greatly attenuated following electrolytic as well as chemical destruction of the parabrachial region. On the other hand, when the PAG was extensively lesioned, baroreflex inhibition produced by hypothalamic defense area stimulation was markedly diminished. PAG excitation thus causes powerful inhibition of arterial baroreflexes which is mediated by the parabrachial region; the PAG also mediates a major fraction of hypothalamic inhibition of the baroreflexes.

Anesthesia↗
PubMed1993

Spontaneous baroreflex by sequence and power spectral methods in humans.

Beat-by-beat variations in blood pressure and RR-interval are interrelated by the actions of baroreflex and non-baroreflex responses. This study had two purposes: (1) to examine the spontaneous relationships between RR-interval and systolic blood pressure to determine the relative occurrence of baroreflex and non-baroreflex responses in humans, and (2) to compare the beat-sequence method with a cross spectral estimate of the baroreflex response slope. Eight healthy men were studied during 10 h of quiet, seated rest, and six men and three women were studied during rest, rest plus fixed pace breathing, and a cold pressor test. RR-interval and continuous, non-invasive arterial blood pressure were measured with a computerized system. A baroreflex sequence was defined by a series of at least three consecutive heart beats in which systolic pressure and the following RR-interval either both increased or both decreased. A non-baroreflex relationship was defined by sequences of at least three beats by opposite directional changes of RR-interval and systolic pressure of that beat. The results showed that there were approximately 30% as many non-baroreflex compared to baroreflex slopes. Individual subject mean baroreflex and non-baroreflex slopes were highly correlated (r = 0.72, P < 0.001). Absolute slope values were not different, and they were unaffected by time, fixed pace breathing, or cold pressor test. The data showed the relatively simple beat-by-beat sequence method to yield spontaneous baroreflex response slopes that were quantitatively similar to, and highly correlated with (r = 0.85-0.94), baroreflex response slopes calculated by spectral analysis methods.

Adult↗
PubMed1993

Role of AT1 receptors in the resetting of the baroreflex control of heart rate by angiotensin II in the rabbit.

Angiotensin II (Ang II) resets the baroreflex control of heart rate to a higher blood pressure. This action is apparently mediated via Ang II receptors in the area postrema, but it is not known if these are of the AT1 or AT2 subtype. In the present study the effects of losartan, a selective AT1 receptor antagonist, and PD 123319, a selective AT2 antagonist, on the cardiac baroreflex response to Ang II were investigated in conscious rabbits with chronically implanted arterial and venous catheters. Baroreflex curves were generated with intravenous infusions of phenylephrine and nitroprusside (2.6-25 micrograms/kg per min) and analyzed using a four-parameter logistic model to yield their upper and lower plateaus, arterial pressure at the midpoint of the heart rate range (BP50), and slope coefficient. From these four parameters, the gain and range of the baroreflex were calculated. Background intravenous infusion of Ang II at 10 ng/kg per min increased mean arterial pressure by 17 mmHg but did not change heart rate. Ang II shifted the baroreflex curve to the right as indicated by an increase in BP50 from 70.9 +/- 2.0 to 89.3 +/- 2.7 mmHg (P < 0.05), but did not change baroreflex gain significantly. Ang II did not alter the upper plateau of the baroreflex, but decreased the lower plateau from 119.4 +/- 10.3 to 73.6 +/- 11.5 beats per minute (bpm) (P < 0.05), extending the heart rate range by 52.5 bpm. Pretreatment with losartan completely abolished the pressor and cardiac baroreflex responses to Ang II. In contrast, PD 123319 had no effect on these responses. Administration of losartan alone to block endogenous Ang II shifted the baroreflex curve to the left as indicated by a decrease in BP50 from 71.2 +/- 2.7 to 64.7 +/- 2.5 mmHg (P < 0.05). These results demonstrate that the resetting of the baroreflex control of heart rate by Ang II is mediated by AT1 receptors, and that basal levels of endogenous Ang II exert a tonic action on the cardiac baroreflex to increase the setpoint around which the baroreflex regulates heart rate.

Angiotensin II↗
PubMed1995

Baroreflex sensitivity and neurohormonal activation in patients with acute myocardial infarction.

OBJECTIVE: To examine the relationship between baroreflex sensitivity and neurohormonal activation in patients with an acute myocardial infarction. METHODS: Baroreflex sensitivity, plasma noradrenaline, atrial natriuretic factor, endothelin-1, and plasma renin activity were measured in 37 male patients about 10 days after their first myocardial infarction, and in 15 healthy controls. Baroreflex sensitivity was assessed from the regression line relating the change in RR interval to the change in systolic blood pressure following an intravenous bolus injection of phenylephrine. The measurements were repeated after a follow up of three months. RESULTS: There was a significant inverse correlation between baroreflex sensitivity and plasma noradrenaline measured before hospital discharge (r = -0.43, P < 0.01). Patients with increased plasma noradrenaline (> or = 2SD above the mean of the age matched control group) had significantly lower baroreflex sensitivity than patients with normal plasma noradrenaline (8.7 (SD 4.6) v 12.1 (6.1) ms/mm Hg, P < 0.05). The change in baroreflex sensitivity during the follow up showed a significant inverse correlation with the change of plasma noradrenaline (r = -0.450, P < 0.01). Furthermore, when patients with increased plasma noradrenaline before hospital discharge were analysed separately, baroreflex sensitivity at three months in patients in whom plasma noradrenaline had decreased to normal values was significantly higher than in patients in whom plasma noradrenaline had remained increased (14.6 (5.7) v 8.1 (8.1) ms/mm Hg, P < 0.05). On the other hand, baroreflex sensitivity was not related to the levels of plasma atrial natriuretic factor, plasma endothelin-1, or plasma renin activity. Neither was any relationship found between change in baroreflex sensitivity and change in plasma atrial natriuretic factor, endothelin-1, or plasma renin activity during the follow up. CONCLUSIONS: The impairment baroreflex sensitivity after myocardial infarction was associated with increased concentration of plasma noradrenaline, that is, sympathetic activation, but not with plasma atrial natriuretic factor, endothelin-1, or plasma renin activity. Baroreflex sensitivity provides information about cardiac vagal control as well as about the balance of cardiac sympathetic-parasympathetic regulation.

Adult↗
PubMed1990

Analysis of the action of angiotensin II on the baroreflex control of heart rate in conscious rabbits.

There is considerable evidence that angiotensin II (Ang II) attenuates the baroreflex control of heart rate (HR), but the mechanism and site of this action have not been precisely defined. In the present study the effects of systemically and centrally administered Ang II on the baroreflex control of HR were investigated in conscious, chronically prepared rabbits. Baroreflex curves (HR vs. mean arterial pressure) were generated with iv infusions of phenylephrine or nitroprusside. Background infusion of Ang II at 10 ng/kg.min increased mean arterial pressure from 77.3 +/- 3.0 to 94.3 +/- 4.1 mm Hg (P less than 0.001) without changing HR [212.1 +/- 7.2 to 218.0 +/- 9.8 beats/min (bpm)] and shifted (reset) the baroreflex curve with phenylephrine to a higher pressure level (P less than 0.001) without changing its slope (-1.40 +/- 0.40 to -1.65 +/- 0.46 bpm/mm Hg; P = 0.4). Background infusion of an equipressor dose of phenylephrine did not shift the baroreflex curve or change its slope. Ang II also shifted the baroreflex curve with nitroprusside to a higher pressure level (P less than 0.01), but again the slope was not significantly changed (-2.30 +/- 1.25 to -1.51 +/- 0.52 bpm/mm Hg; P = 0.2). Background intraventricular infusion of Ang II at 1 ng/kg.min had the same effects as iv infusion of Ang II at 10 ng/kg.min; the curve was shifted to a higher pressure level (P less than 0.001), but the slope was not changed (-0.76 +/- 0.47 to -1.143 +/- 0.48 bpm/mm Hg). Intravenous infusion of Ang II at 1 ng/kg.min had no effect on the baroreflex. The resetting of the baroreflex with phenylephrine by iv Ang II (10 ng/kg.min) was not blocked by propranolol: atropine markedly reduced the baroreflex response to phenylephrine in both the absence and presence of Ang II. These results indicate that in conscious rabbits, Ang II resets the baroreflex control of HR, but does not change its sensitivity. This effect apparently results from an action of Ang II on the brain that is mediated by withdrawal of vagal tone to the heart. The resetting of the baroreflex by Ang II can explain the ability of the peptide to increase arterial pressure without decreasing HR.

Angiotensin II↗
PubMed1996

Enalaprilat augments arterial and cardiopulmonary baroreflex control of sympathetic nerve activity in patients with heart failure.

OBJECTIVES: This study sought to determine the effects of enalaprilat on reflex control of sympathetic nerve activity. BACKGROUND: Angiotensin-converting enzyme inhibitors decrease mortality in patients with congestive heart failure. Their efficacy appears to be related importantly to antiadrenergic effects, the mechanism for which has not been determined. Because baroreflexes tonically inhibit sympathetic outflow, and baroreflexes are blunted in heart failure, we hypothesized that these agents reduce sympathetic activity by augmenting baroreflexes. METHODS: We assessed baroreflex control of sympathetic nerve activity and heart rate in patients with congestive heart failure and in control subjects before and after enalaprilat (0.02 mg/kg body weight intravenously). Arterial baroreflexes were perturbed by bolus administration of sodium nitroprusside and phenylephrine. Cardiopulmonary baroreflexes were perturbed by lower body negative pressure and head-down tilt. Muscle sympathetic nerve activity was recorded by microneurography. RESULTS: Enalaprilat decreased systolic blood pressure in patients with heart failure and control subjects. Sympathetic nerve activity increased in control subjects but decreased in patients with heart failure after enalaprilat despite reductions in central venous pressure in this group. Baroreflex control of sympathetic nerve activity was unchanged by enalaprilat in control subjects. In patients with heart failure, both arterial and cardiopulmonary baroreflex control of sympathetic nerve activity was enhanced by enalaprilat. Baroreflex control of heart rate was unchanged by enalaprilat in either group. CONCLUSIONS: Enalaprilat augments both arterial and cardiopulmonary baroreflex control of sympathetic activity in heart failure. These augmented inhibitory influences are associated with a reduction in sympathetic outflow and may contribute to the beneficial effects of angiotensin-converting enzyme inhibitors in heart failure.

Adult↗
PubMed1995

Renal sympathetic and heart rate baroreflex function in conscious and isoflurane anaesthetized normotensive and chronically hypertensive rabbits.

1. Baroreflex control of heart rate (HR) has been studied in normotensive (NT) and hypertensive (HT) awake and anaesthetized animals and man, but baroreflex control of sympathetic nerve activity has not been well studied. We investigated baroreflex control of HR and renal sympathetic nerve activity (RSNA) over a wide range of arterial pressure (AP) in conscious and isoflurane (ISO) anaesthetized NT and HT rabbits. 2. Animals were instrumented to record AP, HR and RSNA. Hypertension was accomplished by renal encapsulation. AP-HR and AP-RSNA baroreflex function curves were obtained while awake and after 1.0, 1.5, 2.0 and 2.5% ISO. All baroreflex curves were fit to sigmoid or exponential functions. 3. In conscious rabbits, HT for 3-5 weeks, AP was significantly higher (75.6 +/- 0.8 vs 102.3 +/- 8.9 mmHg); HR significantly lower (218.0 +/- 5.5 vs 189.5 +/- 5.5 beats/min); and RSNA not different than NT rabbits (14.9 +/- 2.2 vs 9.9 +/- 3.2% max RSNA). 4. ISO shifted AP-HR and AP-RSNA baroreflex curves to the left in NT and HT animals, and significantly attenuated baroreflex range and slope. At low ISO concentrations, baroreflex compensation for decreases in AP is limited to small increases in HR and sympathetic nerve activity. At higher ISO concentrations, baroreflex responses to decreases in AP are lost. RSNA responses to increases in AP are preserved with increasing ISO concentrations while HR responses are progressively attenuated. The sole effect of chronic hypertension was to shift the AP-HR and AP-RSNA barocurves to the right along the pressure axis in both conscious and ISO anaesthetized animals with no additional change in range or slope. 5. At this stage of hypertension development, ISO anaesthesia affects baroreflex function equally in normotensive and hypertensive rabbits.

Analysis of Variance↗
PubMed1996

Effects of NO on baroreflex control of heart rate and renal nerve activity in conscious rabbits.

Recent data suggest that nitric oxide (NO) plays a role in the modulation of sympathetic nerve activity and baroreflex sensitivity. Most of these studies have been carried out in anesthetized preparations, and little if any comparison has been made on the relative role of NO on the baroreflex control of heart rate and sympathetic nerve activity. In the present studies, the effect of the NO synthase inhibitor NG-nitro-L-arginine (L-NNA) on the baroreflex control of heart rate (HR) and renal sympathetic nerve activity (RSNA) were investigated in conscious, instrumented rabbits. Intravenous bolus injections of 13 mg/kg of L-NNA decreased baseline HR (from 205.0 +/- 6.0 to 145.5 +/- 8.2 beats/min; P < 0.05) without significant changes in mean arterial pressure (MAP) and RSNA. L-NNA significantly reduced the lower plateau of the HR-MAP curves and increased the sensitivities of baroreflex control of HR and RSNA. L-Arginine (600 mg/kg i.v.) but not D-arginine reversed the above effects. The effects of L-NNA on baseline HR were not completely blocked by metoprolol (2 mg/kg) or by atropine (0.2 mg/kg). After pretreatment with metoprolol, baroreflex sensitivity was reduced and L-NNA increased baroreflex sensitivity back to the control level. After pretreatment with atropine, L-NNA still reduced the lower plateau but did not significantly affect baroreflex sensitivity. L-NNA increased the HR responses but not the RSNA response to electrical stimulation of the aortic nerve in chloralose-anesthetized, sinoaortic-denervated (SAD) rabbits. L-NNA had no effect on the HR response to right vagal stimulation. In both conscious intact and SAD rabbits, L-NNA did not increase baseline RSNA. These results suggest that endogenous NO decreases baroreflex control of HR and RSNA. Both sympathetic and parasympathetic components play a role in the effects of NO on the baroreflex control of HR. The effects of NO in the central nervous system play a more important role in the baroreflex control of HR than of RSNA.

Animals↗
PubMed1980

Baroreflex sensitivity in renal failure.

1. Baroreflex sensitivity was evaluated in 22 non-dialysed patients with chronic renal failure secondary to chronic glomerulonephritis. Baroreflex sensitivity was judged by the slope of the linear regression of the pulse interval on the rise in systolic blood pressure with injection of phenylephrine or reduction by amyl nitrite inhalation. 2. Baroreflex sensitivity was reduced in these patients as compared with normal controls. Reduction of baroreflex sensitivity was significantly greater in nine hypertensive than 13 normotensive patients with chronic renal failure. 3. A significant positive correlation was found between baroreflex sensitivity and motor nerve conduction velocity measured on ulnar nerve in 13 patients examined. 4. Saline was given with high dietary salt intake to seven normotensive patients with chronic renal failure for 2 or 5 days in order to determine whether the severe depression of baroreflex sensitivity can be an initiating factor for hypertension. Blood pressure was raised to hypertensive levels within 5 days in two patients in whom baroreflex sensitivity was nearly as low as that of hypertensive patients, but not in five cases whose baroreflex sensitivity was normal or only mildly depressed. Plasma volume increased to the same degree in both groups. Baroreflex sensitivity did not change in the former two cases despite blood pressure elevation. 5. It is concluded that reduced baroreflex sensitivity in chronic renal failure correlated with the prescence ofhypertension, as well as uraemic neuropathy, and may be one of the pathogenetic mechanisms of hypertension in end-stage chronic glomerulonephritis.

Adult↗
PubMed1992

Baroreflex sensitivity and heredity in essential hypertension.

BACKGROUND: Abnormalities in baroreflex control of heart rate may be important in the pathogenesis of essential hypertension. METHODS AND RESULTS: To investigate the influence of heredity on baroreflex function, we measured baroreflex sensitivity in 40 untreated patients with essential hypertension grouped by the presence (FH+) or absence (FH-) of a family history of hypertension and in 24 normotensive counterparts. Baroreflex sensitivity was assessed by both high-pressure (phenylephrine bolus) and low-pressure (amyl nitrite inhalation) stimuli. Subject groups were matched for age, blood pressure, body weight, and race. Baroreflex sensitivity (in milliseconds per millimeter of mercury) assessed by amyl nitrite inhalation was 24.3 +/- 2.8 in FH- normotensives, 12.3 +/- 1.7 in FH+ normotensives, 15.4 +/- 3.3 in FH- hypertensives, and 8.1 +/- 1.2 in FH+ hypertensives. Baroreflex sensitivity assessed by phenylephrine bolus was 28.8 +/- 5.6 in FH- normotensives, 19.3 +/- 2.8 in FH+ normotensives, 19.1 +/- 2.0 in FH- hypertensives, and 13.6 +/- 1.3 in FH+ hypertensives. Two-factor analysis of variance showed significant effects on baroreflex sensitivity for blood pressure status (normotensive versus hypertensive) and for family history of hypertension. After control line (controlling) for the effects of several variables, including age, mean arterial pressure, body weight, and race through multiple linear regression analysis, the effect of family history of hypertension on baroreflex sensitivity was still highly significant. Indeed, of all variables investigated, family history of hypertension was the strongest unique baroreflex sensitivity predictor. CONCLUSIONS: These data suggest that the impairment in baroreflex sensitivity in hypertension is in part genetically determined and may be an important hereditary component in the pathogenesis of essential hypertension.

Administration, Inhalation↗
PubMed1990

Role of the area postrema in the modulation of the baroreflex control of heart rate by angiotensin II.

During angiotensin II (Ang II)-induced elevation of arterial pressure, there is an attenuation of the baroreflex control of heart rate (HR), but the site of this action of Ang II on the baroreflex is not known. To investigate the role of the area postrema, the effects of Ang II on arterial pressure and HR and on the baroreflex control of HR were compared in intact and area postrema-lesioned conscious rabbits. In intact rabbits, infusion of Ang II (2.5-100 ng/kg/min) produced dose-related increases in mean arterial pressure (MAP); the largest dose increased MAP by 32 +/- 3 mm Hg. HR decreased only at the highest dose of Ang II (21 +/- 6 beats/min). In lesioned rabbits, the increase in MAP was reduced (23 +/- 2 mm Hg, p less than 0.05) while the decrease in HR was enhanced (50 +/- 8 beats/min, p less than 0.01). The pressor and HR responses to infusion of phenylephrine (PE) (2-20 micrograms/kg/min) were not different between the two groups. In intact rabbits, the slope of the relation between HR and MAP during Ang II infusion was less than that during PE infusion; in lesioned rabbits, the slopes were not significantly different. Responses to bolus injections of Ang II and PE in intact and lesioned rabbits were similar to those obtained in the infusion study. In another series of experiments, cardiac baroreflex responses with or without background infusion of Ang II were obtained by increasing blood pressure with graded infusions of PE (2-20 micrograms/kg/min). In intact rabbits, infusion of Ang II at 10 ng/kg/min shifted the baroreflex to a higher pressure level (resetting) without changing its slope (sensitivity). Background infusion of PE caused comparable increases in blood pressure, but the subsequent baroreflex response was identical to the response without background PE. In lesioned rabbits, background infusion of Ang II did not change the slope, nor did it reset the baroreflex. The effects of Ang II on baroreflex responses during nitroprusside infusions (2-20 micrograms/kg/min) in intact and lesioned rabbits were the same as those observed during the PE infusions. These findings indicate that the attenuation of the baroreflex control of HR by Ang II results from resetting of the cardiac baroreflex and suggest that this effect is mediated via the area postrema.

Angiotensin II↗
PubMed1994

Role of endogenous ANG II on resetting arterial baroreflex during development.

Angiotensin II (ANG II) has been shown in adults to modulate baroreflex responses in heart rate (HR) and sympathetic outflow. To test the hypothesis that high circulating levels of ANG II in the newborn period contribute to the resetting of the arterial baroreflex observed postnatally, we studied baroreflex-mediated changes in HR and renal sympathetic nerve activity (RSNA) before and after angiotensin-converting enzyme (ACE) inhibition in fetal and newborn sheep. In the newborn, administration of the ACE inhibitor enalaprilat produced significant (P < 0.05) decreases in baseline RSNA (69 +/- 5 vs. 47 +/- 7% maximum) and HR (81 +/- 3 vs. 59 +/- 4% max), as well as in the baroreflex curve midpoints for RSNA (93 +/- 4 vs. 87 +/- 3 mmHg) and HR (95 +/- 4 vs. 81 +/- 5 mmHg); no change in the sensitivities (gains) of the baroreflex responses were seen. In contrast, no significant changes in baseline RSNA, HR, baroreflex curve midpoint, or sensitivity were demonstrated in the fetus. Infusion of ANG II in newborn lambs reversed the effects of ACE inhibition on the baroreflex responses. Additional experiments evaluating the effects of ACE inhibition in vagotomized newborns again showed resetting of the baroreflex, demonstrating that vagally mediated mechanisms are not involved in regulating the changes in sympathetic outflow during the neonatal period. These results suggest that endogenous ANG II contributes to the resetting of the baroreflex observed postnatally.

Angiotensin II↗