Estrogen enhancement of baroreflex sensitivity  is centrally mediated

We have recently shown that estrogen enhances baroreceptor control of reflex bradycardia in conscious rats. The present study replicated this finding in pentobarbital sodium-anesthetized rats, and the study was extended to investigate whether this effect of estrogen is centrally or peripherally mediated. Hemodynamic responses to electrical stimulation of the central end of the aortic depressor or the vagal efferent nerve were evaluated in pentobarbital sodium-anesthetized sham-operated (SO), ovariectomized (OVX), and OVX estradiol-treated Sprague-Dawley rats. Phenylephrine (1–16 μg/kg iv) elicited dose-dependent pressor and bradycardic responses. Regression analysis of the baroreflex curves, relating changes in mean arterial pressure and heart rate, revealed a significantly smaller baroreflex sensitivity in OVX compared with SO anesthetized rats (−0.54 ± 0.05 and −0.91 ± 0.12 beats ⋅ min−1 ⋅ mmHg−1, respectively; P < 0.05). Treatment of OVX rats with 17β-estradiol (E2, 50 μg ⋅ kg−1 ⋅ day−1for 2 days subcutaneously) significantly enhanced baroreflex sensitivity to a level similar to that of SO rats ( P < 0.05). The enhancing effect of E2 on the baroreflex-mediated bradycardia, observed in conscious and anesthetized rats, seems to be selective because the baroreflex-mediated tachycardic responses measured in a separate group of conscious rats were not altered by ovariectomy or E2 administration. Electrical stimulation of the aortic nerve elicited frequency-dependent depressor and bradycardic responses that were significantly smaller in OVX compared with SO values ( P < 0.05). Treatment of OVX rats with E2 restored the hemodynamic responses to aortic stimulation to near SO levels. On the other hand, hemodynamic responses to vagal stimulation were not affected by OVX or treatment with E2. These findings suggest that enhancement of reflex bradycardia by estrogen is centrally mediated and involves interaction with central projections of the aortic nerve.

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Role of periaqueductal gray in the pressor response produced by central injections of angiotensin II

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1993.265.5.r1052 ◽

1993 ◽

Vol 265 (5) ◽

pp. R1052-R1059

Author(s):

L. R. Portis ◽

S. J. Lewis ◽

M. J. Brody

Keyword(s):

Electrical Stimulation ◽

Angiotensin Ii ◽

Fluorescent Dyes ◽

Pressor Response ◽

Periaqueductal Gray ◽

Ang Ii ◽

Hemodynamic Responses ◽

Anesthetized Rats ◽

Stimulation Of

The present studies were undertaken to determine the role of rostral periaqueductal gray (PAG) in mediating the pressor effect produced by intracerebroventricular (icv) injection of angiotensin II (ANG II, 200 ng). Two functionally and anatomically distinct sites were identified in rostral PAG: a dorsomedial site involved in the hemodynamic responses produced by electrical stimulation of the anteroventral third ventricle (AV3V) region and a ventromedial site required for the pressor response elicited by icv administration of ANG II. In Saffan-anesthetized rats, injection of lidocaine (LIDO, 4%) in dorsomedial PAG, but not in ventromedial PAG, significantly attenuated the decrease in hindquarter resistance (HQR) produced by electrical stimulation of the AV3V region, and the poststimulatory increase in mean arterial pressure (MAP) and HQR. The injection of LIDO in ventromedial PAG had no effect on the hemodynamic responses produced by electrical stimulation of the AV3V region in anesthetized rats but significantly attenuated the pressor response produced by icv administration of ANG II in conscious rats. The hypothesis that these two sites receive separate projections was addressed by microinjecting two retrogradely transported fluorescent dyes, Fluoro-Gold and Fast Blue. The anatomic findings suggest that separation of the pathways activated by electrical and chemical stimulation of the AV3V region occurs at the level of rostral PAG.

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Abstract 032: Carotid Chemoreceptor Activation Blunts The Hypotensive Response Caused By The Electrical Stimulation Of The Carotid Sinus In Conscious Rats

Hypertension ◽

10.1161/hyp.64.suppl_1.032 ◽

2014 ◽

Vol 64 (suppl_1) ◽

Author(s):

Pedro L Katayama ◽

Jaci A Castania ◽

Rubens Fazan ◽

Helio C Salgado

Keyword(s):

Electrical Stimulation ◽

Resistant Hypertension ◽

Carotid Sinus ◽

Hemodynamic Responses ◽

Carotid Chemoreceptors ◽

Conscious Rats ◽

Carotid Baroreceptors ◽

Bilateral Carotid ◽

Hypotensive Response ◽

Stimulation Of

The mechanisms involved in Baroreflex Activation Therapy (BAT) in patients with resistant hypertension require better understanding. It was shown that electrical stimulation of the carotid sinus (ESCS), in conscious carotid body-denervated rats, caused bradycardia and greater hypotensive response when compared with intact control rats. In the current study the activation of the chemoreceptors due to ESCS, in conscious rats, was examined in the absence of the carotid baroreceptors. Wistar rats with unilateral denervation of the right carotid chemoreceptors were divided into three groups: 1) control (CONT, n=7); 2) bilateral carotid chemoreceptor denervation (CD, n=7); 3) unilateral denervation of the left carotid baroreceptors (BD, n=4). Under ketamine/xylazine anesthesia bipolar electrodes were implanted around the left carotid sinus combined with arterial and venous catheters into the femoral vessels. On the next day, after basal hemodynamic recordings, the animals received three ESCS (5V, 1 ms) with 15 Hz, 30 Hz and 60 Hz, applied randomly for 20s. Carotid chemoreceptors denervation was confirmed by the lack of hemodynamic responses after the administration of KCN (40 μg iv). The efficacy of left carotid baroreceptor denervation was confirmed by the absence of hemodynamic responses to changes in the left carotid sinus pressure ranging from 60 mmHg to 180 mmHg. The results showed that ESCS was efficient to cause greater hypotensive responses in the CD as compared with the CONT group at 60 Hz (-37 ± 6 vs -19 ± 3 mmHg) and to cause hypertensive responses in the BD group at 30 Hz and 60 Hz (15 ± 2 and 19 ± 2 mmHg). ESCS caused no alteration of the heart rate in the CONT but caused significant bradycardia in the CD group at 30 Hz and 60 Hz (-31 ± 11 and -35 ± 12 bpm) and in the BD group at 15 Hz, 30 Hz and 60 Hz (-38 ± 6, -37 ± 6 and -34 ± 4 bpm). These data demonstrated that carotid chemoreceptor activation in the absence of the carotid baroreceptors caused hypertension and bradycardia, indicating that when the baroreceptors are intact, the chemoreceptors blunt the hypotensive response caused by ESCS. These findings provide important information for the clinical studies using BAT in patients with resistant hypertension and/or heart failure.

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Sympathetic responses to stimulation of area postrema in decerebrate and anesthetized rats

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1995.268.3.h1086 ◽

1995 ◽

Vol 268 (3) ◽

pp. H1086-H1095 ◽

Cited By ~ 2

Author(s):

A. A. Hegarty ◽

L. F. Hayward ◽

R. B. Felder

Keyword(s):

Electrical Stimulation ◽

Excitatory Amino Acid ◽

Area Postrema ◽

Neuronal Cell ◽

Renal Sympathetic Nerve Activity ◽

Pentobarbital Sodium ◽

Anesthetized Rats ◽

Neuronal Cell Bodies ◽

Decerebrate Rat ◽

Stimulation Of

The effects of electrical and chemical stimulation of the area postrema (AP) on mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA) were examined in urethan- and pentobarbital sodium-anesthetized rats and in unanesthetized decerebrate rats. The AP was electrically stimulated over a range of frequencies (10–100 Hz) and intensities (10–80 microA) with a pulse duration of 0.2 or 1.0 ms. The excitatory amino acid L-glutamate (100 or 200 mM) was microinjected into the AP to preferentially stimulate neuronal cell bodies. In urethan-anesthetized rats, electrical stimulation of the AP decreased MAP and RSNA. In pentobarbital sodium-anesthetized rats, MAP and RSNA were markedly increased by AP stimulation. In unanesthetized decerebrate rats, increases in MAP and RSNA were also observed during electrical AP stimulation. Microinjection of L-glutamate had no effect on MAP and RSNA in anesthetized or in unanesthetized rats. These results indicate that electrical AP stimulation increases sympathetic output in the unanesthetized decerebrate rat and that anesthesia modifies this sympathetic response. The findings also suggest that peripheral responses to L-glutamate and electrical stimulation of the AP are mediated over different central pathways.

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