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Baroreflex Gain (baroreflex + gain)

Distribution by Scientific Domains

Medical Sciences	60%

Selected Abstracts

The baroreflex is counteracted by autoregulation, thereby preventing circulatory instability

EXPERIMENTAL PHYSIOLOGY, Issue 4 2004
Roberto Burattini
The aims of this study were (a) to apply in the animal with intact baroreflex a two-point method for estimation of overall, effective open-loop gain, G0e, which results from the combined action of baroregulation and total systemic autoregulation on peripheral resistance; (b) to predict specific baroreflex gain by correcting the effective gain for the autoregulation gain; and (c) to discuss why the effective gain is usually as low as 1,2 units. G0e was estimated from two measurements of both cardiac output, Q, and mean systemic arterial pressure, P: one in the reference state (set-point) and the other in a steady-state reached 1,3 min after a small cardiac output perturbation. In anaesthetized cats and dogs a cardiac output perturbation was accomplished by partial occlusion of the inferior vena cava and by cardiac pacing, respectively. Average (±s.e.m.) estimates of G0e were 1.4 ± 0.2 (n= 8) in the cat and 1.5 ± 0.4 (n= 5) in the dog. The specific baroreflex open-loop gain, G0b, found after correction for total systemic autoregulation, was 3.3 ± 0.4 in the cat and 2.8 ± 0.8 in the dog. A model-based analysis showed that, with G0e as low as 1.4, the closed-loop response of P to a stepwise perturbation in Q results in damped oscillations that disappear in about 1 min. The amplitude and duration of these oscillations, which have a frequency of about 0.1 Hz, increase with increasing G0e and cause instability when G0e is about 3. We conclude that autoregulation reduces the effectiveness of baroreflex gain by about 55%, thereby preventing instability of blood pressure response. [source]

Role of Myocardial Contractility and Autonomic Control in the Hypotensive Response to a Limited Access Ethanol Paradigm in SHRs

ALCOHOLISM, Issue 6 2007
Mahmoud M. El-Mas
Background: Previous experimental studies that evaluated the chronic hemodynamic effect of ethanol employed the continuous exposure protocol of ethanol, which does not mimic the pattern of alcohol consumption in humans. This study dealt with the long-term hemodynamic and cardiovascular autonomic effects of ethanol, in a limited-access regimen in telemetered spontaneously hypertensive rats (SHRs). Methods: Changes in blood pressure (BP), heart rate (HR), myocardial contractility (dP/dtmax), and spectral cardiovascular autonomic profiles during the ethanol exposure period (2.5 or 5% w/v, 8 h/d, 8:30 am till 4:30 pm) were followed for 12 weeks. Results: Compared with control pair-fed SHRs, body weight and urine output, osmolality, and potassium levels were decreased in SHRs receiving 5% but not 2.5% ethanol. Blood pressure showed progressive falls during ethanol-feeding periods with a maximum effect observed at week 5. The peak hypotensive effect was maintained thereafter in SHRs receiving 5% ethanol in contrast to steady rises in BP in the 2.5% ethanol group to near-control levels by the conclusion of the study. Heart rate was slightly but significantly increased by ethanol 5% whereas dP/dtmax showed persistent reductions. Power spectral analysis showed that ethanol attenuated the baroreflex gain of HR as suggested by the reductions in index ,, the spectral index of spontaneous baroreflex sensitivity (BRS). Conclusions: It is concluded that limited access ethanol drinking in SHRs elicited hypotension that was concentration dependent and mediated, at least partly, through reductions in myocardial contractility. Baroreflex sensitivity attenuation by ethanol appeared to have limited the tachycardic response to ethanol and perhaps its capacity to offset the evoked hypotension. [source]

Adrenomedullin in the rostral ventrolateral medulla inhibits baroreflex control of heart rate: a role for protein kinase A

BRITISH JOURNAL OF PHARMACOLOGY, Issue 1 2006
Yong Xu
1The rostral ventrolateral medulla (RVLM) is an essential vasomotor center in the brainstem which participates in maintaining resting levels of arterial pressure and for regulating baroreflex activity. We have demonstrated that microinjections of adrenomedullin (ADM), a vasoactive neuropeptide, into the RVLM cause increased resting mean arterial pressure (MAP) and heart rate (HR). However, the effect of ADM on baroreflex function remains unclear. 2The purposes of the present study were to investigate the effect of ADM in the RVLM on the regulation of baroreflex activity and to identify the underlying mechanisms. Baroreflex curves were generated with intravenous injections of multiple doses of phenylephrine and nitroprusside. The upper and lower plateaus, reflex range, MAP at the midpoint of HR range (MAP50), and gain were evaluated before and after various microinjections were made into the RVLM of urethane-anesthetized rats. 3Microinjections of ADM decreased the upper plateau, reflex range, and gain, and increased MAP50, indicating that ADM in the RVLM impairs baroreflex function. 4ADM22,52, a putative ADM receptor antagonist, significantly increased the baroreflex gain and upper plateau, demonstrating that endogenous ADM tonically inhibits the baroreflex. Coinjections of ADM22,52 with ADM blocked the ADM-induced baroreflex responses. 5ADM's effect was abolished with H-89, a protein kinase A (PKA) inhibitor. 6Our results show that ADM in the RVLM exerts an inhibitory effect on baroreflex activity via an ADM receptor-mediated mechanism, and that activation of PKA is involved in this event. British Journal of Pharmacology (2006) 148, 70,77. doi:10.1038/sj.bjp.0706698 [source]

Renal And Cardiac Sympathetic Baroreflexes In Hypertensive Rabbits

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 12 2001
Geoffrey A Head
SUMMARY 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. [source]