Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Baroreflex”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 55 records · Page 3Linked to original sources
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↗
PubMed2005

Carotid endarterectomy impairs blood pressure homeostasis by reducing the physiologic baroreflex reserve.

OBJECTIVE: To assess the impact of carotid endarterectomy on blood pressure homeostasis and baroreflex function, with particular reference to the presence or absence of significant contralateral carotid artery disease, we conducted a prospective study in 80 patients with symptomatic extracranial carotid disease undergoing carotid endarterectomy in a regional teaching hospital over 2 years. METHODS: Patients were divided into two groups: the control group (n = 37) had no significant contralateral carotid disease; patients in the diseased group (n = 23) had either >70% stenosis or occlusion of the contralateral carotid artery. Seventeen patients with abnormal heart rhythms, poor quality recordings, or with intermediate degrees of contralateral carotid stenosis were excluded. Three patients who had previously undergone contralateral carotid endarterectomy were separately evaluated. Atheromatous plaque was removed from carotid lumen and the baroreflex mechanism received direct intraoperative stimulation before and after carotid endarterectomy. The main outcome measures were (1) the hemodynamic response to the carotid endarterectomy, baroreflex sensitivity, and operating set point (the resting blood pressure, which the baroreflex mechanism maintains) before and after removal of the atheromatous plaque, and (2) the responsiveness of the ipsilateral baroreceptor mechanism to direct stimulation. The impact of the presence of contralateral carotid stenosis on these variables was also evaluated. RESULTS: Patients in the two groups were comparable for preoperative demographic, medication, and hemodynamic variables. Carotid endarterectomy led to a rise in mean arterial pressure from 81.3 +/- 3.9 mm Hg to 103.5 +/- 4.6 mm Hg ( P < .00001) and from 87.6 +/- 4.3 mm Hg to 94.0 +/- 4.5 mm Hg ( P < .003) in the diseased and control groups, respectively. The magnitude of blood pressure response was significantly greater in the diseased group than in the control group ( P < .00001). This hypertensive shift was not accompanied by the expected fall in heart rate. Direct baroreflex stimulation prior to carotid endarterectomy caused a significantly greater response in the diseased group, suggesting sensitization of the ipsilateral carotid baroreceptor in the presence of contralateral carotid disease. Furthermore, the baroreflex response was obliterated after endarterectomy. There were significant reductions in baroreflex sensitivity and a hypertensive shift in the operating set point, the magnitude of which was significantly greater in patients with contralateral carotid disease. CONCLUSIONS: Carotid endarterectomy impairs blood pressure homeostasis through surgical destruction of the ipsilateral carotid baroreflex mechanism. Patients with contralateral carotid stenosis have a reduced baroreflex reserve and show greater baroreflex dysfunction and hemodynamic instability after endarterectomy. These patients are at greater risk of postendarterectomy complications and should be monitored closely.

Aged↗
PubMed2006

Baroreflex mechanisms in major depression.

BACKGROUND: Recent studies have shown that depressive disorder is associated with impaired baroreceptor or baroreflex sensitivity, which is proposed to be a predisposing factor for sudden death in patients with manifest cardiac disease. These studies have not evaluated the afferent and efferent components of the cardiac baroreflex loop or other baroreflex mechanisms that regulate target processes (cardiac metabolism and blood pressure variability) related to the impairment. The objective of this study was to gain more insight into autonomic functioning in depressive disorder to more fully examine the potential basis for increased cardiac mortality. METHODS: The subjects were 28 women and men with unipolar major depression who were taking antidepressant medications and who were in partial remission and free of cardiovascular or other serious disease, and 28 healthy control subjects matched for sex, age, and ethnicity. The two samples were compared for negative affective dispositions (anger expression, hostility, defensiveness, anxiety), spontaneous (closed-loop) baroreflex activity, heart rate, heart rate variability, systolic blood pressure, and heart rate-systolic blood pressure double product under resting conditions. RESULTS: Depressed patients showed a general disposition to anger suppression coupled with higher hostility and anxiety, and lower defensiveness. The patients showed higher general sympathetic activity (high levels of blood pressure, low-frequency heart rate variability) and lower parasympathetic-related activity (high heart rate and reduced high frequency heart rate variability) with affected cardiac metabolism estimated by the double product. Depressed patients had lower baroreflex sensitivity related to a higher gain of the afferent component of the baroreflex without respective gain adjustment of its efferent component (reflex gain 'de-afferentation'). It was coupled with a compensatory higher number of effective baroreflex reactions (reflex gating 're-afferentation'). Antidepressant agents and depressed mood had additional independent effects on baroreflex sensitivity through the efferent component of the cardiac baroreflex loop. CONCLUSIONS: The data indicate that different baroreflex components and mechanisms may be impaired in patients with depression and may contribute to their increased cardiac risk.

Adult↗
PubMed2001

Renal and cardiac sympathetic baroreflexes in hypertensive rabbits.

1. The purpose of the present study was to assess the changes to renal sympathetic nerve activity (RSNA) baroreflexes during the development of hypertension after renal clipping in conscious rabbits. 2. Rabbits were fitted with a clip on the right renal artery or underwent a sham operation under halothane anaesthesia. A recording electrode was implanted on the left renal nerve 1 week before the experiment, 3 or 6 weeks after the initial operation. During the experiment, drug-induced ramp rises and falls in mean arterial pressure (MAP) were used to produce RSNA and heart rate (HR) baroreflex curves. The RSNA for each experiment was calibrated against maximum RSNA evoked by stimulation of baroreceptor-independent trigeminal afferents. 3. Mean arterial pressure was 20 and 36% higher 3 and 6 weeks after clip implantation, respectively. Renal sympathetic nerve activity baroreflex curves were reset rightwards accordingly, but the shape of the RSNA curves was differentially affected. 4. At both hypertensive periods, MAP-HR baroreflex gain was markedly reduced due to a reduction in curvature. The HR baroreflex range was increased. The RSNA baroreflex gain was reduced at 3 weeks, which was due to a 35% lower RSNA baroreflex range, but was similar to sham animals at 6 weeks. 5. The results show that, in established two kidney, one clip hypertension in rabbits, the sympathetic baroreflex is relatively well preserved but sensitivity of cardiac baroreflexes is attenuated. Therefore, the short-term inhibition of RSNA baroreflexes is not related to the level of blood pressure or the development of secondary changes, such as cardiac or vascular hypertrophy, but may be related to circulating angiotensin, which is known to increase at this time.

Animals↗
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↗
PubMed1998

Noninvasive assessment of spontaneous baroreflex sensitivity in patients with liver cirrhosis.

AIMS/BACKGROUND: An impairment of baroreceptor sensitivity has been found in liver cirrhosis. Noninvasive and spontaneous estimates of baroreflex sensitivity are obtained from beat-to-beat blood pressure and heart rate recordings by means of cross-spectrum analysis and calculation of alpha-index (as a measure of baroreflex gain). The aim of the present study was to investigate the function of the spontaneous baroreflex sensitivity related to clinical Child score in liver cirrhosis. METHODS: The alpha-index was evaluated in 40 cirrhotic patients (18 with and 22 without ascites) and 17 healthy subjects by analysing finger arterial pressure recorded noninvasively with the Portapres device. RESULTS: Baroreflex sensitivity was significantly lower in cirrhotic patients with and without ascites compared with healthy subjects (p<0.01). Furthermore, in patients with ascites the baroreflex gain was significantly related to plasma sodium (p<0.01). A significant inverse relationship was present between baroreflex gain and grade of Child score and the severity of ascites (p<0.01). There were no significant relationships between hormonal parameters (catecholamines, renin, aldosterone, arginine-vasopressin, atrial natriuretic peptide and nitric oxide) and baroreflex gain. No significant differences were found between healthy subjects and cirrhotic patients with respect to systolic and diastolic blood pressure total variability in a supine position, whilst it was lower in cirrhotic patients with ascites in a tilted position (p<0.05). CONCLUSION: Our findings showed that baroreflex sensitivity was significantly impaired in cirrhotic patients when compared with healthy subjects. In addition, there was a significant trend toward lower baroreflex sensitivity values with the grade score of Child class (p<0.01). Spectral analysis of the alpha-index provides viable alternatives to the pharmacological approach for estimation of baroreflex sensitivity and may represent a prognostic tool to identify cirrhotic patients at increased risk of adverse events.

Aldosterone↗
PubMed2003

Nociception attenuates parasympathetic but not sympathetic baroreflex via NK1 receptors in the rat nucleus tractus solitarii.

Somatic noxious stimulation can evoke profound cardiovascular responses by altering activity in the autonomic nervous system. This noxious stimulation attenuates the cardiac vagal baroreflex, a key cardiovascular homeostatic reflex. This attenuation is mediated via NK1 receptors expressed on GABAergic interneurones within the nucleus of the solitary tract (NTS). We have investigated the effect of noxious stimulation and exogenous substance P (SP) on the sympathetic component of the baroreflex. We recorded from the sympathetic chain in a decerebrate, artificially perfused rat preparation. Noxious hindlimb pinch was without effect on the sympathetic baroreflex although the cardiac vagal baroreflex gain was decreased (56 %, P < 0.01). Bilateral NTS microinjection of SP (500 fmol) produced a similar selective attenuation of the cardiac vagal baroreflex gain (62 %, P < 0.005) without effect on the sympathetic baroreflex. Recordings from the cardiac sympathetic and vagal nerves confirmed the selectivity of the SP inhibition. Control experiments using a GABAA receptor agonist, isoguvacine, indicated that both components of the baroreflex (parasympathetic and sympathetic) could be blocked from the NTS injection site. The NTS microinjection of a NK1 antagonist (CP-99,994) in vivo attenuated the tachycardic response to hindlimb pinch. Our data suggest that noxious pinch releases SP within the NTS to selectively attenuate the cardiac vagal, but not the sympathetic, component of the baroreflex. This selective withdrawal of the cardiac vagal baroreflex seems to underlie the pinch-evoked tachycardia seen in vivo. Further, these findings confirm that baroreflex sympathetic and parasympathetic pathways diverge, and can be independently controlled, within the NTS.

Animals↗
PubMed2006

Hierarchical recruitment of the sympathetic and parasympathetic limbs of the baroreflex in normotensive and spontaneously hypertensive rats.

The arterial baroreflex acts to buffer acute changes in blood pressure by reciprocal modulation of sympathetic and parasympathetic activity that controls the heart and vasculature. We have examined the baroreflex pressure-function curves for changes in heart rate and non-cardiac sympathetic nerve activity (SNA, thoracic chain T8-12) in artificially perfused in situ rat preparations. We found that the non-cardiac SNA baroreflex is active over a lower range of pressures than the cardiac baroreflex (threshold 66 +/- 1 mmHg versus 82 +/- 5 mmHg and mid-point 77 +/- 3 versus 87 +/- 4 mmHg, respectively, P < 0.05, n = 6). This can manifest as a complete dissociation of the baroreflex limbs at low pressures. This difference between the cardiac and non-cardiac SNA baroreflex is also seen in end-organ sympathetic outflows (adrenal and renal nerves). Recordings of the cardiac vagal (parasympathetic) and the inferior cardiac (sympathetic) nerves identify the cardiac parasympathetic baroreflex component as being active over a higher range of pressures. This difference in the operating range of the baroreflex-function curves is exaggerated in the spontaneously hypertensive rat where the cardiac component has selectively reset by 20-25 mmHg to a higher pressure range (threshold of 104 +/- 4 mmHg and mid-point 113 +/- 4, n = 6). The difference in the pressure-function curves for the cardiac versus the vascular baroreflex indicates that there is a hierarchical recruitment of the output limbs of the baroreflex with a sympathetic predominance at lower arterial pressures.

Animals↗
PubMed2003

Effect of blockade of endogenous angiotensin II on baroreflex function in conscious diabetic rats.

Little is known about baroreflex control of renal nerve sympathetic activity (RSNA) or the effect of angiotensin II (ANG II) on the baroreflex in diabetes. We examined baroreflex control of RSNA and heart rate (HR) in conscious, chronically instrumented rats 2 wk after citrate vehicle (normal) or 55 mg/kg iv streptozotocin (diabetic) before and after losartan (5 mg/kg iv) or enalapril (2.5 mg/kg iv). Resting HR and RSNA were lower in diabetic versus normal rats. The range of baroreflex control of HR and the gain of baroreflex-mediated bradycardia were impaired in diabetic rats. Maximum gain was unchanged. The baroreflex control of RSNA was reset to lower pressures in the diabetic rats but remained otherwise unchanged. Losartan decreased mean arterial pressure (MAP) and increased HR and RSNA in both groups but had no influence on the baroreflex. Enalapril decreased MAP only in normal rats, yet the increase in HR and RSNA was similar in both groups. Thus in diabetic rats enalapril produced a pressure-independent increase in HR and RSNA. Enalapril exerted no effect on the baroreflex control of HR or RSNA in either group. These data indicate that in conscious rats resting RSNA is lower but baroreflex control of RSNA is preserved after 2 wk of diabetes. At this time, the baroreflex control of HR is already impaired and blockade of endogenous ANG II does not improve this dysfunction.

Angiotensin II↗
PubMed1999

ANG II and baroreflex function in rabbits with CHF and lesions of the area postrema.

Blockade of the angiotensin II (ANG II) type 1 receptor (AT(1)) has been shown to restore baroreflex sensitivity in rats and rabbits with experimental chronic heart failure (CHF). Because the modulation of baroreflex function in response to ANG II is mediated in part by AT(1) receptors located in the area postrema, we hypothesized that lesions of the area postrema would prevent the enhancement in baroreflex function in response to AT(1)-receptor blockade in rabbits with pacing-induced CHF. Experiments were carried out on 24 male New Zealand White rabbits that were divided into sham (n = 12) and lesioned (n = 12) groups further divided into normal and CHF subgroups (n = 6 each). All rabbits were identically instrumented to measure cardiac external dimensions, central venous pressure, arterial pressure, heart rate (HR), and renal sympathetic nerve activity (RSNA). After 3-4 wk of pacing, baroreflex sensitivity (infusions of phenylephrine and nitroprusside) was evaluated before and after intravenous administration of the AT(1)-receptor antagonist L-158,809. Maximum baroreflex sensitivity in nonpaced rabbits was 5.4 +/- 0.7 beats. min(-1). mmHg(-1) and 5.2 +/- 0.5% of maximum/mmHg for HR and RSNA curves, respectively, and was not altered by L-158,809 in either intact or lesioned rabbits. In contrast, L-158,809 enhanced baroreflex sensitivity in intact rabbits with CHF (HR from 1.6 +/- 0.3 to 4.1 +/- 0.7 beats. min(-1). mmHg(-1), P < 0.001; RSNA from 2.3 +/- 0.2 to 4.9 +/- 0.4% of maximum/mmHg, P < 0.001). However, in CHF rabbits with area postrema lesions, L-158,809 failed to enhance baroreflex sensitivity. Interestingly, area postrema lesions did not normalize the baroreflex in CHF rabbits. From these data we conclude that the area postrema mediates the normalization of baroreflex sensitivity after AT(1) blockade in rabbits with CHF but does not modify resting baroreflex function.

Angiotensin II↗
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↗
PubMed2003

Evaluation of baroreflex sensitivity by the sequence method using blood pressure oscillations and R-R interval changes during deep respiration.

BACKGROUND: Baroreflex sensitivity assessments have been considered to be important to evaluate cardiac autonomic neuropathy. The phenylephrine method, Valsalva maneuver or sequence method at rest caused several problems. We evaluated the usefulness of the sequence method during deep respiration. METHOD: Baroreflex sensitivity was evaluated in 20 normal volunteers and 50 patients with Parkinson's disease. R-R intervals and systolic blood pressures were obtained by electrocardiogram and tonometry using a continuous blood pressure monitoring system. The sequence method is an evaluation of baroreflex sensitivity using sequences of 3 or more consecutive beats for 4 min. Baroreflex sensitivity was also assessed by the Valsalva maneuver at 5 beats before the peak systolic blood pressure of phase IV. The slope of the linear interrelationship between systolic blood pressure and the following R-R interval, i.e. baroreflex sensitivity (ms/mm Hg), was calculated with a correlation coefficient greater than 0.8. RESULT: The mean value of baroreflex sensitivity obtained by the Valsalva maneuver was 7.91 in normal volunteers and 5.35 in patients with Parkinson's disease; the one obtained by the sequence method at rest was 9.10 in normal volunteers and 8.42 in patients with Parkinson's disease, and the one obtained by the sequence method during deep respiration was 10.23 in normal volunteers and 6.73 in patients with Parkinson's disease. In some cases with Parkinson's disease, baroreflex sensitivities could not be found, whereas in all patients with Parkinson's disease, the sequence method during deep respiration could be used for evaluations. Significant correlations were found among the baroreflex sensitivities obtained by the Valsalva maneuver, and the sequence method at rest or during deep respiration in normal volunteers and patients with Parkinson's disease. CONCLUSIONS: The baroreflex sensitivity obtained by the sequence method during deep respiration could be investigated noninvasively in all cases with PD, being thus a useful method for clinical evaluation of baroreflex sensitivity.

Aged↗
PubMed2004

Alpha-2 adrenergic transmission and human baroreflex regulation.

We observed earlier that central alpha-2 adrenoceptor stimulation in mice greatly augments parasympathetic tone. To test the effects in humans, we assessed autonomic vasomotor tone and baroreflex regulation in 9 normal young adults on 2 occasions, once with and once without clonidine. We determined heart rate (HR), beat-by-beat blood pressure (BP), and muscle sympathetic nerve activity. HR variability was analyzed in the time and frequency domain. Pharmacological baroreflex slopes were determined using incremental phenylephrine and nitroprusside infusions. Clonidine lowered resting BP (122+/-4/73+/-3 versus 100+/-7/55+/-3 mm Hg, P<0.01), muscle sympathetic nerve activity (18+/-3 versus 4+/-2 bursts/min, P<0.01), and HR (62+/-3 versus 56+/-3 bpm, P<0.05). The baroreflex heart rate curve was reset to much lower HR values and showed no saturation at low HR. HR variability profoundly increased during clonidine plus phenylephrine (total power: 3224+/-843 versus 8943+/-2329 ms2, P<0.05). High-frequency power was 1451+/-520 at baseline and 6720+/-2475 ms2 during baroreceptor loading (P<0.05). The low-frequency/high-frequency ratio decreased (1.94+/-0.41 versus 0.69+/-0.10, P<0.05). In contrast, clonidine reduced resting sympathetic vasomotor tone and shifted the operating point of the sympathetic baroreflex to a flat part of the sympathetic baroreflex curve. The shift decreased the ability of the baroreflex to withdraw sympathetic vasomotor tone during baroreflex loading. These baroreflex changes were associated with a moderate increase in phenylephrine responsiveness. We conclude that alpha-2 adrenoceptor stimulation has a differential effect on baroreflex HR and vasomotor regulation. alpha-2 Adrenoceptor stimulation greatly augments baroreflex-mediated bradycardia, most likely by parasympathetic activation.

Action Potentials↗
PubMed2003

Heat stress modifies human baroreflex function independently of heat-induced hypovolemia.

Since human thermoregulatory heat loss responses, cutaneous vasodilation and sweating, cause hypovolemia, they should resultantly stimulate human baroreflexes. However, it is possible that the thermoregulatory system directly interacts with the baroreflex system through central neural connections independently of the heat-induced hypovolemia. We hypothesized that heat stress modifies the baroreflex control of sympathetic nerve activity independently of heat-induced hypovolemia in humans. We made whole-body heating with tube-lined suits perfused with warm water (46-47 degrees C) on 10 healthy male subjects. The heating increased skin and tympanic temperatures by 10.0 and 0.4 degrees C, respectively. It increased resting total muscle sympathetic nerve activity (MSNA, microneurography) by 94 +/- 9% and decreased central venous pressure (CVP, dependent arm technique) by 2.6 +/- 0.9 mmHg. The heating increased arterial baroreflex gain by 193%, assessed as a response of MSNA to a decrease in diastolic arterial pressure during Valsalva's maneuver, but it did not change threshold arterial pressure for MSNA activation. Although the heating did not change the cardiopulmonary baroreflex gain assessed as a response of MSNA to a change in estimated central venous pressure (CVP) during a 10 degrees head-down and -up tilt test, it upwardly shifted the stimulus-response baroreflex relationship. These changes in baroreflex functions during heating were not restored by an intravenous infusion of warmed isotonic saline (37 degrees C, 15 ml/kg) that restored the heat-induced reduction of CVP. Our results support our hypothesis that heat stress modifies the baroreflex control of MSNA independently of heat-induced hypovolemia in humans. Our results also suggest that the hyperthermal modification of baroreflex results from central neural interaction between thermoregulatory and baroreflex systems.

Adult↗
PubMed1998

[Spontaneous baroreflex control of heart rate during chronic tandropril therapy].

Differently from other vasodilators, the antihypertensive effect of ACE-inhibitors is not accompanied by an increase in resting heart rate which suggests a modulatory action of these drugs on arterial baroreflex control of heart rate. It is debated whether this modulation involve, an increase in gain (or sensitivity) of baroreflex mechanisms controlling heart rate or is due to a baroreflex control resetting. In this study we investigated the arterial baroreflex control of heart rate both in supine rest and during active standing before and after 7 and 30 days of treatment with a new ACE-inhibitor, trandolapril (2 mg per os oid) in 15 mild hypertensive patients. Baroreflex control of heart rate has been dynamically and non-invasively assessed by analysis of the continuous relationship between beat-to-beat spontaneous fluctuations in systolic blood pressure and pulse interval. By this method, sequences of 3 or more consecutive beats in which systolic blood pressure and pulse interval change in the same direction (either increasing or decreasing) are identified and a linear regression is applied to each individual sequence. The mean individual slope of the systolic blood pressure/pulse interval ratio obtained by averaging all slopes computed within a given period, is calculated and taken as an estimate of the spontaneous baroreflex sensitivity for that period. Trandolapril reduced resting blood pressure significantly (from 147.5 +/- 3.3/95.3 +/- 1.5 to 129.5 +/- 3.7/83.6 +/- 1.6 and 126.6 +/- 3.9/84.5 +/- 1.7 mmHg after 7 e 30 days, respectively) without affecting heart rate. The treatment did not alter baroreflex sensitivity but resulted in an apparent leftward shift of the regression line relating systolic blood pressure to pulse interval along the pressure axis, reflecting the lower prevailing level of arterial pressure. The increases in heart rate and blood pressure induced by standing in control conditions were not significantly modified by trandolapril. Baroreflex sensitivity was significantly reduced by standing both in control conditions and, to the same extent, during treatment. These results suggest that ACE-inhibition does not alter the gain of the integrated baroreflex mechanisms controlling heart rate, but results in a baroreflex resetting that may explain the lack of tachycardia normally observed during antihypertensive therapy with ACE-inhibitors.

Angiotensin-Converting Enzyme Inhibitors↗
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↗
PubMed1997

Acute and chronic effects of exercise on baroreflexes in spontaneously hypertensive rats.

We studied the effects of acute and chronic exercise on the arterial baroreflex and chemosensitive cardiopulmonary baroreflex (CCB) in spontaneously hypertensive rats (SHR). Arterial baroreflex and CCB were evaluated in normotensive rats (NR, n=11) and SHR (n=5) at rest and after 30 minutes of an acute bout of exercise (45 minutes at 50% of VO2max). In addition, these baroreflexes were evaluated in sedentary (n=5) and exercise-trained (n=9) SHR. Exercise training was performed on a motor treadmill, 5 days/week, during 60 minutes, at 50% of VO2max. Baroreflex bradycardia and tachycardia, analyzed by baroreflex sensitivity index (delta heart rate/delta mean arterial pressure), were significantly lower in SHR than in NR (0.7+/-0.1 versus 2.0+/-0.1 and 1.8+/-0.2 versus 3.4+/-0.1 beats per minute [bpm]/mm Hg, respectively). During the recovery period from acute exercise, baroreflex bradycardia was significantly higher than at rest only in SHR (1.7+/-0.1 versus 0.7+/-0.1 bpm/mm Hg). Hypotension and bradycardia induced by CCB stimulation (5-hydroxytryptamine, I.V.) were similar between SHR and NR, and an acute exercise bout did not change these responses. Exercise training markedly improved baroreflex bradycardia and tachycardia in SHR (1.9+/-0.1 versus 0.7+/-0.1 and 2.9+/-0.1 versus 1.8+/-0.2 bpm/mm Hg, respectively). Exercise-trained rats had greater bradycardiac (118+/-26 versus 14+/-2 and 209+/-30 versus 19+/-5 bpm to 1 and 2 microg/kg 5-HT, respectively) and hypotensive (30+/-6 versus 15+/-3 and 45+/-7 versus 17+/-2 mm Hg to 1 and 2 microg/kg 5-hydroxytryptamine, respectively) responses to CCB stimulation. In conclusion, an acute bout of exercise increases baroreflex bradycardia in SHR, and exercise training attenuates hypertension concomitant with improved arterial baroreflex and CCB sensitivity in SHR.

Animals↗