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PubMed2003

Ontogeny of baroreflex control in the American alligator Alligator mississippiensis.

Baroreflex regulation appears in different species at different points in embryonic development. This study was designed to understand the development of the baroreflex in embryos of the American alligator at four different points of embryonic development (60%, 70%, 80% and 90% of a total incubation period of 72 days) and in 1-week-old hatchlings. Data from a separate study on 1-year-old alligators were included for comparison. The gain of the cardiac limb of the baroreflex was calculated from heart rate changes triggered by pharmacological manipulation of arterial pressure with sodium nitroprusside and phenylephrine. The results demonstrated that a vagally mediated hypertensive baroreflex was present during the final 30% of alligator development. A hypotensive baroreflex was not present in embryos but appeared in hatchlings, mediated by a combined effect of vagal and sympathetic efferents. Absolute baroreflex gain was maximal at 80% of incubation (41.22 beats kPa(-1) min(-1)) and dropped thereafter, reaching a minimum in 1-year-old alligators (9.69 beats kPa(-1) min(-1)). When the baroreflex gain was normalized to resting arterial pressure and heart rate, the maximum gain was observed in 1-year-old alligators (normalized index of 2.12 versus 0.75 in hatchlings and 0.69 as the highest gain in embryos). In conclusion, baroreflex regulation appeared during embryonic development with a substantial gain. These findings indicate that embryonic development is a period of preparation for cardiovascular regulatory mechanisms that will be necessary in adult life and that the baroreflex control mechanism is required for cardiovascular control during ontogeny.

Alligators and Crocodiles↗
PubMed2006

Carotid-cardiac baroreflex function does not influence blood pressure regulation during head-up tilt in humans.

The influence of the carotid-cardiac baroreflex on blood pressure regulation was evaluated during supine rest and 40 degrees head-up tilt (HUT) in 9 healthy young subjects with and without full cardiac vagal blockade. The carotid baroreflex responsiveness, or maximal gain (G(MAX)), was assessed from the beat-to-beat changes in heart rate (HR) and mean arterial pressure (MAP) by the variable neck pressure and suction technique ranging in pressure from +40 to -80 Torr, with and without glycopyrrolate (12.0 +/- 1.0 microg/kg body weight; mean +/- SE). In the supine position, glycopyrrolate increased the HR to 91 +/- 3 bpm, from 54 +/- 3; MAP to 89 +/- 2 mmHg, from 76 +/- 2; and cardiac output to 6.8 +/- 0.3 l.min(-1), from 4.9 +/- 0.3 (P < 0.05). The G(MAX) of the carotid baroreflex control of HR was reduced to -0.06 +/- 0.01 bpm.mmHg(-1), from -0.30 +/- 0.02 (P < 0.05) with no significant effect on the G(MAX) of the carotid baroreflex control of MAP. During HUT the carotid baroreflex control of MAP was unchanged, though the G(MAX) of the carotid baroreflex control of HR was increased (P < 0.05). During HUT, central blood volume, assessed by electrical thoracic admittance, and total vascular conductance were decreased with and without glycopyrrolate. Furthermore, glycopyrrolate reduced G(MAX) of the carotid baroreflex control of HR during HUT (P < 0.05) with no significant effect on G(MAX) of the carotid baroreflex control of MAP. These data suggest that during supine rest and HUT-induced decreases in central blood volume, the carotid baroreflex control of HR is mediated primarily via parasympathetic activity. Furthermore, the maintenance of arterial blood pressure during postural stress is primarily mediated by arterial and cardiopulmonary reflex regulation of sympathetic activity and its effects on the systemic vasculature.

Adult↗
PubMed2000

Baroreflex control of heart rate in young and adult salt hypertensive inbred Dahl rats.

Baroreflex control of heart rate was studied in inbred salt-sensitive (SS/Jr) and salt-resistant (SR/Jr) Dahl rats that were subjected to chronic dietary sodium chloride loading (for 4 weeks) either in youth or only in adulthood, i.e. from the age of 4 or 12 weeks. Using phenylephrine administration to pentobarbital-anesthetized male rats we have demonstrated the decreased baroreflex sensitivity (lower slope for reflex bradycardia) in young prehypertensive SS/Jr rats fed a low-salt diet as compared to age-matched SR/Jr animals. High salt intake further suppressed baroreflex sensitivity in young SS/Jr but not in SR/Jr rats. Baroreflex sensitivity decreased with age in SR/Jr rats, whereas it increased in SS/Jr rats fed a low-salt diet. Thus at the age of 16 weeks baroreflex sensitivity was much higher in SS/Jr than in SR/Jr animals. High salt intake lowered baroreflex sensitivity even in adult SS/Jr rats without affecting it in adult SR/Jr rats. Nevertheless, baroreflex sensitivity was significantly lower in young SS/Jr rats with a severe salt hypertension than in adult ones with a moderate blood pressure elevation. It is concluded that the alterations of baroreflex sensitivity in young inbred SS/Jr rats (including the response to high salt intake) are similar to those described earlier for outbred salt-sensitive Dahl rats. We have, however, disclosed contrasting age-dependent changes of baroreflex sensitivity in both inbred substrains of Dahl rats.

Age Factors↗
PubMed1988

Baroreflex sensitivity and its evolution during the first year after myocardial infarction.

Experimental data have indicated that baroreflex sensitivity is often depressed in dogs after myocardial infarction and that this depression correlates strongly with subsequent mortality during episodes of acute myocardial ischemia. This finding has several clinical implications. The present study was undertaken with the objectives of assessing the potential existence of differences in baroreflex sensitivity between men with and without myocardial infarction and the time course during the 1st year after infarction of these potential changes in baroreflex sensitivity. Fifty-three subjects entered the study: 32 postinfarction patients and 21 control subjects. Baroreflex sensitivity was assessed by increasing mean blood pressure by aphenylephrine infusion (70 micrograms/ml) and recording the consequent RR interval changes. Baroreflex sensitivity, expressed as the slope of the regression line relating mean blood pressure to RR interval changes, was evaluated 18 days (n = 32), 3 months (n = 17) and 13 months (n = 10) after infarction. Baroreflex sensitivity was lower in the patients than in the control subjects (8.2 +/- 3.7 versus 12.3 +/- 2.9 ms/mm Hg, p = 0.0001). Moreover, 13 (41%) of 32 patients had a baroreflex slope less than 6.5 ms/mm Hg, which was 2 SD below the mean value of the control subjects. The internal control follow-up study showed that baroreflex sensitivity increased 3 months after infarction to values quite similar to those observed in the control subjects (11.1 +/- 5.3 versus 8.7 +/- 3.5 ms/mm Hg, p = 0.02). No further change was observed between 3 and 13 months after myocardial infarction. These data indicate that baroreflex sensitivity is lower in a proportion of postinfarction patients than in control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1978

Effects of propranolol on baroreflex sensitivity in borderline hypertension.

Patients with borderline hypertension have reduced baroreflex sensitivity, but the mechanism is not known. These patients reportedly have increased beta-adrenergic activity. Since beta-adrenergic activity has been reported to antagonise baroreflex sensitivity, this study was undertaken, first to determine if propranolol increases baroreflex sensitivity in borderline hypertension, and secondly to test the hypothesis that increased beta-adrenergic activity might contribute to reduced baroreflex sensitivity in these patients. The effect of beta-adrenergic blockade on baroreflex sensitivity was studied in 11 patients with borderline hypertension and was compared with that of six age-matched control subjects. Baroreflex sensitivity was significantly increased by propranolol, 0.2 mg.kg-1 intravenously, in patients with borderline hypertension. However, after propranolol baroreflex sensitivity was still lower in the patients with borderline hypertension than it was in control subjects (P less than 0.01). The results suggest, first that increased beta-adrenergic activity is not a major factor contributing to decreased baroreflex sensitivity in borderline hypertension and, second that increased baroreflex sensitivity produced by propranolol might contribute to the anti-hypertensive effect of this drug.

Adolescent↗
PubMed1991

Depression of baroreflex control of heart rate by halothane in growing piglets.

The purpose this study was to examine the effects of halothane on baroreflex control of heart rate in developing swine. Serial tests of baroreflex function were performed over the first 2 months of life in eight piglets in the conscious state and during anesthesia with 0.45, 0.9, and 1.35% halothane. Systemic blood pressure was increased with phenylephrine (pressor test) and decreased with nitroprusside (depressor test), and stimulus-response curves relating mean blood pressure to heart rate were constructed. Baroreflex sensitivity was determined as the slope of the linear portion of the curve. Halothane markedly depressed baroreflex sensitivity at all ages in a dose-dependent manner (conscious greater than 0.45% greater than 0.9%, 1.35%). Increasing age was accompanied by decreasing baroreflex sensitivity in both the conscious and the anesthetized states. The difference in baroreflex sensitivity between conscious and anesthetized states did not change with age for the depressor test (tachycardia response), but it did change with age for the pressor test (bradycardia response). For this test, conscious values converged toward anesthetized values at higher ages; therefore, there was relatively less depression by halothane at older ages. Halothane also decreased resting heart rate and decreased the limits and narrowed the range of the baroreflex heart rate response. Increasing age was accompanied by a decreasing resting heart rate and by decreasing limits and a narrowing range of the baroreflex response. The effect of halothane on heart rate variables was similar at all ages. Halothane decreased resting blood pressure and decreased the lower limit and widened the span of the baroreflex blood pressure range.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2000

Bupivacaine inhibits baroreflex control of heart rate in conscious rats.

BACKGROUND: Because exposure to intravenously administered bupivacaine may alter cardiovascular reflexes, the authors examined bupivacaine actions on baroreflex control of heart rate in conscious rats. METHODS: Baroreflex sensitivity (pulse interval vs. systolic blood pressure in ms/mmHg) was determined before, and 1.5 and 15.0 min after rapid intravenous administration of bupivacaine (0.5, 1.0, and 2.0 mg/kg) using heart rate changes evoked by intravenously administered phenylephrine or nitroprusside. The actions on the sympathetic and parasympathetic autonomic divisions of the baroreflex were tested in the presence of a muscarinic antagonist methyl atropine and a beta-adrenergic antagonist atenolol. RESULTS: Within seconds of injection of bupivacaine, mean arterial pressure increased and heart rate decreased in a dose-dependent manner. Baroreflex sensitivity was unaltered after administration of 0.5 mg/kg bupivacaine. In addition, 1 mg/kg bupivacaine at 1.5 min depressed phenylephrine-evoked reflex bradycardia (0.776 +/- 0.325 vs. 0.543 +/- 0.282 ms/mmHg, P < 0.05) but had no effect on nitroprusside-induced tachycardia. Bupivacaine (2 mg/kg), however, depressed reflex bradycardia and tachycardia (phenylephrine, 0.751 +/- 0.318 vs. 0.451 +/- 0.265; nitroprusside, 0.839 +/- 0.256 vs. 0.564 +/- 0.19 ms/mmHg, P < 0.05). Baroreflex sensitivity returned to prebupivacaine levels by 15 min. Bupivacaine (2 mg/kg), in the presence of atenolol, depressed baroreflex sensitivity (phenylephrine, 0.633 +/- 0.204 vs. 0.277 +/- 0.282; nitroprusside, 0.653 +/- 0.142 vs. 0.320 +/- 0.299 ms/mmHg, P < 0.05). In contrast, bupivacaine did not alter baroreflex sensitivity in the presence of methyl atropine. CONCLUSIONS: Bupivacaine, in clinically relevant concentrations, inhibits baroreflex control of heart rate in conscious rats. This inhibition appears to involve primarily vagal components of the baroreflex-heart rate pathways.

Anesthetics, Local↗
PubMed1992

Prognostic value of baroreflex sensitivity testing after acute myocardial infarction.

BACKGROUND: Disturbances of autonomic function are recognised in both the acute and convalescent phases of myocardial infarction. Recent studies have suggested that disordered autonomic function, particularly the loss of protective vagal reflexes, is associated with an increased incidence of arrhythmic deaths. The purpose of this study was to compare the value of differing prognostic indicators with measures of autonomic function and to assess the safety of arterial baroreflex testing early after infarction. METHODS: As part of a prospective trial of risk stratification in post-infarction patients arterial baroreflex sensitivity, heart rate variability, long term electrocardiographic recordings, exercise stress testing, and ejection fraction were recorded between days 7 and 10 in 122 patients with acute myocardial infarction. RESULTS: During a one year follow up period there were 10 arrhythmic events. Baroreflex sensitivity was appreciably reduced in these patients suffering arrhythmic events (1.73 SD (1.49) v 7.83 (4.5) ms/mm hg, 95% confidence interval (CI) 4.8 to 7.3, p = 0.0001). Significant correlations were noted with age (r = -0.68, p less than 0.001) but not left ventricular function. When baroreflex sensitivity was adjusted for the effects of age and ventricular function baroreflex sensitivity was still considerably reduced in the arrhythmic group (2.1 v 7.57 ms/mm Hg, p less than 0.0001). Depressed baroreflex sensitivity carried the highest relative risk for arrhythmic events (23.1, 95% CI 7.7 to 69.2) and was superior to other prognostic variables including left ventricular function (10.4, 95% CI 3.3 to 32.6) and heart rate variability (10.1, 95% CI 5.6 to 18.1). No major complications were noted with baroreflex testing and in particular no patients developed ischaemic or arrhythmic symptoms during the procedure. CONCLUSIONS: Disordered autonomic function as measured by depressed baroreflex sensitivity or reduced heart rate variability was associated with an increase incidence of arrhythmic events in post-infarction patients. Baroreflex testing can be safely performed in the immediate post-infarction period.

Adult↗
PubMed1989

Arterial baroreflex abnormalities in heart failure. Reversal after orthotopic cardiac transplantation.

Arterial baroreflex control of the heart and peripheral circulation is markedly impaired in humans and animals with congestive heart failure. After reversal of heart failure in animal models, arterial baroreflex control of heart rate remains impaired for up to 8 months. Cardiac transplantation restores normal ventricular function and completely reverses heart failure, but does it normalize arterial baroreflex control of heart rate in humans? We studied baroreflex sensitivity in 11 patients with severe heart failure, six normal control patients, and 23 patients at 2 weeks to 4 years after orthotopic cardiac transplantation. Baroreflex sensitivity was assessed with intravenous bolus injections of phenylephrine and is expressed as change in RR or PP interval (msec) per millimeters of mercury rise in systolic arterial pressure. Atrial rate of both donor (denervated) and recipient (innervated) atria were measured in the transplant group. Baroreflex sensitivity in patients with severe heart failure was 2.0 +/- 0.3 msec/mm Hg, but in patients after cardiac transplantation, it was 13.0 +/- 0.9 msec/mm Hg (p less than 0.001). The responses in the transplant group were similar to those observed in normal controls (10 +/- 1.2 msec/mm Hg, p = NS). Our data indicate that patients with severe congestive heart failure have marked abnormalities of baroreflex control, which are reversed as early as 2 weeks after cardiac transplantation. In view of this rapid reversal, we consider it unlikely that abnormal baroreflex sensitivity seen in heart failure is due to structural alterations in the baroreceptors. We speculate that neurohumoral rather than structural abnormalities account for depressed baroreflex sensitivity in heart failure.

Adult↗
PubMed2006

Arterial baroreflex sensitivity is a good predictor of inotropic responses to a phosphodiesterase inhibitor in human heart failure.

BACKGROUND: Experimental study has shown that blunted arterial baroreflex function markedly attenuated inotropic responses to a phosphodiesterase inhibitor (PDEI) even in normal hearts. However, whether arterial baroreflex function is related to the inotropic responsiveness to a PDEI has not been clarified in human heart failure (HF). HYPOTHESIS: The goal of this study was to examine the relationship between inotropic responses to a PDEI and arterial baroreflex sensitivity in human HF. METHODS: Twelve patients with HF were examined, and hemodynamic responses to milrinone (12.5, 25, and 50 microg/kg, intravenous injection) and arterial baroreflex sensitivity were assessed by pulse interval-left ventricular (LV) systolic pressure slope using nitroglycerin and phenylephrine. RESULTS: Milrinone (25 microg/kg) significantly increased LV dP/dt. Arterial baroreflex sensitivity was only one predictor of inotropic responses to milrinone by multivariate analysis; a strong positive correlation was also found between LV dP/dt and baroreflex sensitivity (y = 6.656X - 3.326, r = 0.93, p = 0.000). CONCLUSION: Inotropic effects of milrinone, a PDEI, correlated significantly with arterial baroreflex sensitivity, suggesting that the more baroreflex function was impaired, the more the inotropic effect of a PDEI was depressed in human HF.

Adult↗
PubMed2000

Baroreflex dysfunction induced by microgravity: potential relevance to postflight orthostatic intolerance.

Microgravity imposes adaptive changes in the human body. This review focuses on the changes in baroreflex function produced by actual spaceflight, or by experimental models that simulate microgravity, e.g., bed rest. We will analyze separately studies involving baroreflexes arising from carotid sinus and aortic arch afferents ("high-pressure baroreceptors"), and cardiopulmonary afferents ("low-pressure receptors"). Studies from unrelated laboratories using different techniques have concluded that actual or simulated exposure to microgravity reduces baroreflex function arising from carotid sinus afferents ("carotic-cardiac baroreflex"). The techniques used to study the carotid-cardiac baroreflex, using neck suction and compression to simulate changes in blood pressure, have been extensively validated. In contrast, it is more difficult to selectively study aortic arch or cardiopulmonary baroreceptors. Nonetheless, studies that have examined these baroreceptors suggest that microgravity produces the opposite effect, ie, an increase in the gain of aortic arch and cardiopulmonary baroreflexes. Furthermore, most studies have focus on instantaneous changes in heart rate, which almost exclusively examines the vagal limb of the baroreflex. In comparison, there is limited information about the effect of microgravity on sympathetic function. A substantial proportion of subjects exposed to microgravity develop transient orthostatic intolerance. It has been proposed that alterations in baroreflex function play a role in the orthostatic intolerance induced by microgravity. The evidence in favor and against this hypothesis is reviewed.

Baroreflex↗
PubMed1999

The sympathetic nervous system and baroreflexes in hypertension and hypotension.

Blood pressure and blood volume are closely regulated by the interrelated actions of the sympathetic nervous system (SNS) and the renin-angiotensin-aldosterone system (RAAS). Reflex vasoconstriction caused by parallel SNS and RAAS activation is modulated by two interactive negative feedback systems called baroreflex. The aortic-carotid baroreflex systems respond to momentary changes in systolic blood pressure, adjusting the degree of SNS-dependent peripheral vasoconstriction and cardiac output to allow maintenance of a relatively constant perfusion pressure. Cardiopulmonary baroreflexes respond to momentary changes in cardiac filling, adjusting the degree of peripheral venoconstriction and venous return to maintain cardiac preload and stroke volume. Under normal conditions, each baroreflex system exhibits a degree of tonic negative feedback so that it can alter SNS output immediately, providing counterregulatory increases or decreases in pressure or volume to maintain homeostasis. The SNS is inappropriately active in obesity and hypertension and plays a causal or permissive role in all forms of chronic hypertension. If the negative feedback control exerted by the baroreflexes over the SNS and renin-angiotensin-aldosterone system (RAAS) were perfect, chronic hypertension would not occur. Activity of the baroreflexes, however, is chronically altered by maladaptive changes such as cardiac and vascular fibrosis and hypertrophy. Long-term increases in SNS and RAAS activity also exert ongoing deleterious effects on the heart and vasculature by directly facilitating further cardiac hypertrophy and arterial stiffening. These effects appear to contribute to a vicious cycle of chronic hypertension and target organ damage. Other syndromes of abnormal blood pressure (BP) control, including orthostatic hypotension and baroreflex failure are examples of abnormal baroreflex activity and SNS control.

Animals↗
PubMed1991

Carotid-cardiac baroreflex: relation with orthostatic hypotension following simulated microgravity and implications for development of countermeasures.

In a series of studies, we have examined the effects of exposure to simulated microgravity, varying states of vascular volume, and acute exercise on the function of the carotid-cardiac baroreflex in man. In the first study, exposure to simulated microgravity (6 degrees headdown bedrest) reduced the sensitivity and buffer capacity of the vagal baroreceptor-cardiac reflex mechanisms and this impaired baroreflex function was associated with orthostatic hypotension. Since the reduction in plasma volume during BR was not correlated with impaired baroreflex function, a second study was conducted which demonstrated that the carotid-cardiac baroreflex response was not affected by either acute hypovolemia or hypervolemia. These results suggest that acute fluid replacement prior to reentry may not reverse impaired baroreflex function associated with postflight hypotension. In a third study, we demonstrated that one bout of maximal exercise increased baroreflex sensitivity and buffer capacity through 24 h post-exercise. These baroreflex changes were opposite to those observed following BR. Taken together, these data suggest that the contributions of reduced blood volume and impaired carotid-cardiac baroreflex function to orthostatic hypotension following exposure to microgravity are probably separate and additive; maximal exercise in addition to fluid replacement may provide an acute effective countermeasure against postflight hypotension.

Adult↗
PubMed1993

Effects of acetylstrophanthidin on baroreflex sensitivity in patients with acute myocardial infarction.

We evaluated the effects of acetylstrophanthidin on baroreflex sensitivity in patients soon after an acute myocardial infarction. Baroreflex control of heart rate is frequently depressed after acute myocardial infarction and few data are available as to the effects of pharmacological intervention on this parameter. The reflex chronotropic response to arterial baroreceptor stimulation was assessed in 29 patients with uncomplicated acute myocardial infarction in control conditions (72-96 h after symptom onset) and 30 min after acetylstrophanthidin administration. To check for spontaneous baroreflex sensitivity variations, 24 patients with the same characteristics were evaluated at the same time intervals before and after a 10-cc bolus of saline placebo. Baroreflex sensitivity was assessed by calculating the regression line relating phenylephrine-induced increases in systolic blood pressure to the attendant changes in RR intervals. Mean baseline baroreflex sensitivity value for the whole study population was 7.4 +/- 4.5 ms/mmHg and was unchanged, 7.0 +/- 4.5 ms/mmHg, after acetylstrophanthidin (P = NS). Mean baroreflex sensitivity values were also comparable dividing patients according to the site of infarction both before and after acetylstrophanthidin. Despite the lack of difference in mean baroreflex sensitivity values between the two studies, at a post hoc analysis an inverse relation was found in the total study population between baseline baroreflex sensitivity values and their changes after acetylstrophanthidin (r = -0.62; P < 0.005). The inverse relation was also evident separately in anterior (r = -0.57; P < 0.05) and in inferior (r = -0.70; P < 0.005) myocardial infarction patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2004

Medial prefrontal cortex modulation of the baroreflex parasympathetic component in the rat.

The ventral portion of the medial prefrontal cortex (vMPFC) that comprises the prelimbic and infralimbic cortex is involved in arterial blood pressure and heart rate control. In the present study, we attempted to verify the effect of an acute and reversible blockade of vMPFC activity by local bilateral microinjections of either lidocaine (a local anesthetic) or CoCl2 (a nonselective synapse blocker) on the baroreflex response of unanesthetized rats. Bilateral microinjection of lidocaine into the vMPFC did not affect the tachycardiac response to mean arterial pressure (MAP) decreases caused by i.v. infusion of sodium nitroprusside or the baroreflex gain in unanesthetized rats. However, lidocaine caused a reversible shift of the reflex threshold pressure toward higher (MAP) increases in response to i.v. infusion of phenylephrine, thus indicating an action on the parasympathetic component of the baroreflex. The effects of the blockade of local synapses in the vMPFC by CoCl2 were similar to those observed after the acute ablation of that area caused by lidocaine. Bilateral microinjection of CoCl2 into the vMPFC also caused a shift of the reflex threshold pressure bradycardiac responses to MAP increases toward higher MAP values, without affecting the baroreflex gain. In conclusion, our data indicate that the vMPFC is involved in baroreflex control, and more specifically in the modulation of the parasympathetic baroreflex component. The temporary ablation of this area by local microinjections of lidocaine caused a shift of the reflex threshold pressure toward higher MAP values, which is compatible with the idea that the vMPFC has a modulatory action on the baroreflex. The observation that CoCl2 and lidocaine microinjections had similar effects on the baroreflex also suggests that this modulation involves local synaptic neurotransmission within the vMPFC.

Anesthetics, Local↗
PubMed2006

Blood pressure variability, baroreflex sensitivity and organ damage in spontaneously hypertensive rats treated with various antihypertensive drugs.

Besides blood pressure, blood pressure variability and baroreflex sensitivity maybe important factors determining organ damage in hypertension. This study was designed to investigate the effects of various antihypertensive drugs on blood pressure and blood pressure variability reductions, baroreflex sensitivity, and target organ damage in spontaneously hypertensive rats (SHR). The dose is 20 mg/kg/day for atenolol, and 10 mg/kg/day for nifedipine, irbesartan and hydrochlorothiazide. We used relatively low doses of drugs to avoid a very remarkable normalization of blood pressure in the treatment, which would make it much difficult to distinguish the contribution of blood pressure variability and baroreflex sensitivity to organ protection from that of blood pressure. Drugs at the aforementioned doses were mixed into rat chow. SHR were treated for 4 months. Blood pressure was then continuously recorded for 24 h. After the determination of baroreflex sensitivity, rats were killed for organ-damage evaluation. It was found that long-term treatment with atenolol, nifedipine, irbesartan or hydrochlorothiazide all markedly reduced blood pressure variability, enhanced baroreflex sensitivity, and produced significant organ protection. Compared with blood pressure level, blood pressure variability and baroreflex sensitivity values showed a much closer or similar relationship with organ-damage parameters in every treatment group of rats. Multiple-regression analysis showed that the decrease in left ventricular hypertrophy, the decrease in aortic hypertrophy and the amelioration in renal lesion were all most closely correlated with the increase in baroreflex sensitivity and the decrease in systolic blood pressure variability. In conclusion, long-term treatment with atenolol, nifedipine, irbesartan or hydrochlorothiazide produced organ protection in SHR. Besides the blood pressure reduction, the decrease in blood pressure variability and the restoration of baroreflex sensitivity may contribute to this organ protection.

Animals↗
PubMed1997

Effect of amlodipine on norepinephrine kinetics and baroreflex function in patients with congestive heart failure.

BACKGROUND: The use of calcium channel blocking drugs is controversial in heart failure, partly because of concerns about neurohormonal stimulation. Preliminary data suggest that the newer agent amlodipine may be useful in this syndrome. Suppression of sympathetic activity either directly or by sensitized baroreflex function could be contributing factors to the clinical use of this drug. OBJECTIVE: To assess the effect of short-term amlodipine therapy on baseline measures of sympathetic activity and baroreflex function in patients with chronic stable congestive heart failure (CHF). METHODS: Seven patients with chronic CHF (New York Heart Association functional class II or III, moderate to severe reduction in left ventricular systolic function) were studied. All patients underwent baroreflex testing with head-up tilt, head-down tilt, and head-down tilt with phenylephrine infusion. Heart rate, mean arterial pressure, forearm blood flow and resistance, and plasma norepinephrine (NE) kinetics were assessed at baseline and after each baroreflex perturbation on three occasions: a control test and after 10 days each of placebo and amlodipine therapy. RESULTS: Plasma NE and NE spillover did not significantly increase after amlodipine administration compared with control and placebo tests (488 +/- 119 pg/ml vs 350 +/- 85 and 325 +/- 87 pg/ml). In three subjects, plasma NE levels were essentially unchanged, whereas in four they rose markedly (289 +/- 87 pg/ml at control vs 551 +/- 158 pg/ml). There was no difference in the response of any variable during baroreflex perturbations after amlodipine administration compared with control and placebo tests. One subject who tolerated head-down tilt coupled with phenylephrine administration during the control and placebo tests became markedly short of breath during the same intervention after amlodipine administration. Plasma NE levels in this patient had risen markedly while receiving amlodipine and were not appropriately suppressed during the baroreflex loading maneuver. CONCLUSIONS: Short-term therapy with amlodipine does not suppress sympathetic activity or alter efferent responses to baroreflex perturbation in patients with stable chronic CHF. Significant increases in plasma NE and NE spillover and abnormal responses to baroreflex stimulation are possible after administration of this drug. The relevance of these findings to studies in larger number of patients requires further study.

Aged↗
PubMed1998

Impaired arterial baroreflex regulation of heart rate after blockade of P2-purinoceptors in the nucleus tractus solitarius.

Activation of P2x-purinoceptors in the nucleus tractus solitarius (NTS) via microinjection of ATP mimics baroreflex responses (bradycardia, hypotension); however, the physiological role of these receptors in cardiovascular control remains unclear. We tested whether blockade of these receptors attenuates arterial baroreflex control of heart rate (HR). Baroreflex-induced changes in HR (via graded i.v. infusion of phenylephrine and nitroprusside) were observed in seven alpha-chloralose/urethane anesthetized male Sprague-Dawley rats before and after microinjection of the purinergic P2 receptor antagonist suramin (0.5 nmol in 50 nL) into the subpostremal NTS. Before suramin, typical baroreflex changes in HR were observed (maximum gain, Gmax = 2.94 +/- 0.54 bpm/mmHg). Suramin markedly impaired baroreflex-induced changes in HR (gain = 0.02 +/- 0.08 and 0.18 +/- 0.09 bpm/mmHg for increases and decreases in mean arterial blood pressure, respectively); however, after 90-130 min, HR and baroreflex reactivity returned to control levels. Microinjections of vehicle into the same area did not alter baroreflex function. In addition, suramin did not alter the depressor responses to microinjections of glutamate into the same site of the NTS. We conclude that normal P2x-purinoceptor function in subpostremal NTS may be necessary for baroreflex regulation of HR.

Adenosine Triphosphate↗