Articles: pressoreceptors-physiology.
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J. Pharmacol. Exp. Ther. · May 1986
Central opioid receptors and baroreflex control of sympathetic and cardiovascular function.
The effect of central opioid receptor activation and blockade on arterial baroreflex regulation of cardiovascular function was studied. Baroreceptor reflexes were elicited in urethane-anesthetized rats by graded electrical stimulation of the aortic nerve while mean arterial pressure, heart rate and sympathetic nerve activity were recorded simultaneously. Baroreflex response curves were constructed after intracisternal administration of saline vehicle, after intracisternal infusion of the relatively selective mu and delta opioid receptor agonists D-Ala2-MePhe4-Gly(ol)5 enkephalin (DAGO), or D-Ala2-D-Leu5 enkephalin (DADLE) respectively, and again after i.v. naloxone. ⋯ These results suggest that the effect of DADLE on baroreflexes was mediated by activation of mu rather than delta opioid receptors. No evidence was obtained to suggest a role for endogenous opioid modulation of baroreflexes because i.v. naloxone was without effect. These results demonstrate that activation of central mu opioid receptors significantly impairs baroreflex control of sympathetic and cardiovascular function.
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Circulation research · Oct 1985
The renal sympathetic baroreflex in the rabbit. Arterial and cardiac baroreceptor influences, resetting, and effect of anesthesia.
Curves relating renal sympathetic nerve activity and mean arterial pressure were derived in conscious rabbits during ramp changes in mean arterial pressure, elicited by perivascular balloon inflation. The renal sympathetic nerve activity-mean arterial pressure relationship consisted of a high-gain sigmoidal region about resting, where renal sympathetic nerve activity rose or fell in response to moderate falls and rises of mean arterial pressure. With larger pressure rises, renal sympathetic nerve activity first fell to a lower plateau and then reversed at even higher mean arterial pressure. ⋯ In other experiments, we studied the effects of sustained alterations in resting mean arterial pressure induced by infusing nitroprusside and phenylephrine, which produced rapid resetting of the renal baroreflex. The latter could be accounted for, in part, by resetting of the threshold of the arterial baroreceptors and in part by contributions from other afferents, probably the cardiac receptors. During resetting associated with nitroprusside-induced falls in resting blood pressure, high-gain reflex adjustments in renal sympathetic nerve activity to moderate changes in mean arterial pressure were preserved, but during resetting associated with phenylephrine-induced rises in resting mean mean arterial pressure, the resting renal sympathetic nerve activity lay on the lower curve plateau, resulting in reduction in the apparent gain of the reflex renal sympathetic nerve activity response to moderate changes in mean arterial pressure.
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The baroreceptor reflex has been found to be attenuated during anesthesia, but the effects of the relatively new anesthetic, isoflurane, on baroreflex function have not been examined thoroughly. This study was performed to determine the effects of isoflurane on each component of the baroreceptor reflex arc, including the receptors, afferent and efferent nerve pathways, central integratory centers, peripheral ganglia, and the heart. Baroreflex effects on heart rate initiated by systemic pressure changes were examined in conscious and anesthetized dogs (1.3% and 2.6% isoflurane). ⋯ Cardiac chronotropic responses to direct stimulation of sympathetic and vagal fibers were attenuated significantly by isoflurane, with sympathetic stimulation showing the greater sensitivity to the anesthetic. Carotid baroreceptor afferent activity was increased by isoflurane, and this sensitization of the baroreceptors appeared to contribute to the decreased levels of sympathetic tone. Therefore, although isoflurane was found to alter the baroreceptor reflex through its effects at multiple sites of the baroreflex arc, significant depression of the cardiac chronotropic component of the reflex was seen only at 2.6% isoflurane.
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J. Cardiovasc. Pharmacol. · Sep 1983
Effects of intracisternal and intravenous alpha-methyldopa and clonidine on haemodynamics and baroreceptor--heart rate reflex properties in conscious rabbits.
We determined the doses of intracisternal (i.c.) and intravenous (i.v.) clonidine and alpha-methyldopa (alpha-MD) that produced near-maximal falls in mean arterial pressure (MAP) in conscious rabbits. We then studied the haemodynamic mechanisms underlying the fall in MAP and changes in the properties of the baroreceptor-heart rate reflex. Intracisternal and intravenous administration of both drugs lowered MAP by approximately 25% of control, and the fall was about half due to the reduction in cardiac output and about half due to a fall in total peripheral resistance. ⋯ These differences between drugs were still present with much larger i.c. doses. Our findings suggest that both drugs influence resting haemodynamics and the vagal component of the baroreflex through similar effects on the central autonomic pathways. But there are some differences in their central actions on cardiac sympathetic motoneurons.
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The Journal of physiology · Apr 1983
Effects of acute changes in blood volume on the carotid sinus baroreceptor reflex in conscious rabbits.
The control of blood pressure, heart rate, cardiac output and systemic vascular resistance by the carotid sinus baroreceptor reflex was studied in six conscious rabbits during states of acute hypervolaemia and acute hypovolaemia. These states were produced by infusing blood equal to 20% and 40%, and withdrawing blood equal to 20% and 35%, of the initial blood volume. The properties of the reflex were characterized by creating sinusoidal pressure changes across the wall of the carotid sinus at a frequency of 0.01 Hz and amplitudes of 54 and 83 mmHg. ⋯ The gain for systemic vascular resistance was reduced by hypervolaemia, and increased by 20% hypovolaemia. The gains for heart rate and blood pressure were not affected by hypervolaemia or by 20% hypovolaemia. 35% hypovolaemia reduced the gain for heart rate, but the resting value was close to the upper limit of the reflex response. It also reduced the gain for cardiac output and blood pressure, and the increase in gain for systemic vascular resistance that had been caused by 20% hypovolaemia was not sustained.