Muscle metaboreflex-induced increases in cardiac sympathetic activity vasoconstrict the coronary vasculature.

Muscle metaboreflex-induced increases in cardiac sympathetic activity vasoconstrict the coronary vasculature. Research Abstract Details 

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Muscle metaboreflex-induced increases in cardiac sympathetic activity vasoconstrict the coronary vasculature. Abstract Text:

Donal S O'Leary,Javier A Sala-Mercado,Robert L Hammond,Eric J Ansorge,Jong-Kyung Kim,Jaime Rodriguez,Dominic Fano,Masashi Ichinose,

Ischemia of active skeletal muscle evokes a powerful blood pressure-raising reflex termed the muscle metaboreflex (MMR). MMR activation increases cardiac sympathetic nerve activity, which increases heart rate, ventricular contractility, and cardiac output (CO). However, despite the marked increase in ventricular work, no coronary vasodilation occurs. Using conscious, chronically instrumented dogs, we observed MMR-induced changes in arterial pressure, CO, left circumflex coronary blood flow (CBF), and coronary vascular conductance (CVC) before and after alpha1-receptor blockade (prazosin, 100 microg/kg iv). MMR was activated during mild treadmill exercise by partially reducing hindlimb blood flow. In control experiments, MMR activation caused a substantial pressor response-mediated via increases in CO. Although CBF increased (+28.1 +/- 3.7 ml/min; P < 0.05), CVC did not change (0.45 +/- 0.05 vs. 0.47 +/- 0.06 ml x min(-1) x mmHg(-1), exercise vs. exercise with MMR activation, respectively; P > 0.05). Thus all of the increase in CBF was due to the increase in arterial pressure. In contrast, after prazosin, MMR activation caused a greater increase in CBF (+55.9 +/- 17.1 ml/min; P < 0.05 vs. control) and CVC rose significantly (0.59 +/- 0.08 vs. 0.81 +/- 0.17 ml x min(-1) x mmHg(-1), exercise vs. exercise with MMR activation, respectively; P < 0.05). A greater increase in CO also occurred (+2.01 +/- 0.1 vs. +3.27 +/- 1.1 l/min, control vs. prazosin, respectively; P < 0.05). We conclude that the MMR-induced increases in sympathetic activity to the heart functionally restrain coronary vasodilation, which may limit increases in ventricular function.

Muscle metaboreflex-induced increases in cardiac sympathetic activity vasoconstrict the coronary vasculature. Publishing Authors By Initials

DS O'Leary,JA Sala-Mercado,RL Hammond,EJ Ansorge,JK Kim,J Rodriguez,D Fano,M Ichinose,

For similar circulatory and respiratory physiology: cardiovascular physiology: cardiovascular physiologic processes: ventricular function research abstracts see: circulatory and respiratory physiology: cardiovascular physiology: cardiovascular physiologic processes: ventricular function research

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Muscle metaboreflex-induced increases in cardiac sympathetic activity vasoconstrict the coronary vasculature. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Journal of applied physiology (Bethesda, Md. : 198

VOLUME: 103

Page Numbers: 190-4

Journal Abbreviation: J. Appl. Physiol.

ISSN: 8750-7587

DAY: 3

MONTH: 05

YEAR: 2007

Muscle metaboreflex-induced increases in cardiac sympathetic activity vasoconstrict the coronary vasculature. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 8502536

Muscle metaboreflex-induced increases in cardiac sympathetic activity vasoconstrict the coronary vasculature. Keywords Mesh Terms:

KEYWORDS: Ventricular Function

MESH TERMS: drug effects

Chemical & Substance for Abstract: Muscle metaboreflex-induced increases in cardiac sympathetic activity vasoconstrict the coronary vasculature. Information

Substance Name: Prazosin

Registry Number: 19216-56-9

Grant and Affiliation Information for Muscle metaboreflex-induced increases in cardiac sympathetic activity vasoconstrict the coronary vasculature.

AFFILIATION: Department of Physiology, Wayne State University School of Medicine, Detroit, Michigan 48201, USA. doleary@med.wayne.edu

Country: United States

AGENCY: United States NHLBI

GRANT: HL-55743

ACRONYM: HL

MEDLINETA: J Appl Physiol

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