title: Nonadrenergic noncholinergic nerves regulate basal coronary flow via release of capsaicin-sensitive neuropeptides in the rat heart.
abstract: Nonadrenergic noncholinergic nerve fibers supposedly modulate basal coronary flow by releasing capsaicin-sensitive neuropeptides, but the physiological effects of this intrinsic action have not been clarified. We investigated the intrinsic function of nonadrenergic noncholinergic innervation in modulating basal coronary flow in rats. We administered capsaicin to 44 rats to deplete neuropeptides such as calcitonin gene-related peptide (CGRP) and substance P and administered inert vehicle to 60 control rats. Four days later, we measured the coronary pressure-flow relation in the basal state and during maximal coronary vasodilation induced by intracoronary adenosine administration using Langendorff's method. Changes in basal coronary flow prompted by intracoronary infusion of CGRP or substance P and their antagonists were measured in 54 and 30 rats, respectively. Capsaicin-treated rats showed a 31.5 +/- 0.9% (mean +/- SEM) reduction (P < .01) of basal coronary flow in the range of perfusion pressures between 60 and 140 mm Hg compared with untreated control rats, but the maximal coronary flow after adenosine was similar between the two groups. Although basal coronary flow was reduced in capsaicin-treated hearts, left ventricular contractile force and myocardial oxygen consumption did not fall significantly. CGRP increased the coronary flow, but substance P did not. CGRP(8-37), a CGRP receptor antagonist, reduced basal coronary flow by 24.5 +/- 2.1% (P < .01), but FK888, a substance P antagonist, had little effect on it. Thus, capsaicin-sensitive neuropeptides in the rat heart modulate basal coronary flow, providing approximately 30% of it.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: First Department of Internal Medicine, Fukushima Medical College, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Yaoita
authors.forename: E
authors.initials: E
authors.lastname: Sato
authors.forename: M
authors.initials: M
authors.lastname: Kawaguchi
authors.forename: T
authors.initials: T
authors.lastname: Saito
authors.forename: K
authors.initials: K
authors.lastname: Maehara
authors.forename: Y
authors.initials: Y
authors.lastname: Maruyama
mesh_terms: D000241:Adenosine / Q000494:pharmacology; D000818:Animals; D001341:Autonomic Nervous System / Q000502:physiology*; D015740:Calcitonin Gene-Related Peptide / Q000037:antagonists & inhibitors / Q000502:physiology; D002211:Capsaicin / Q000494:pharmacology*; D003326:Coronary Circulation / Q000187:drug effects; D003331:Coronary Vessels / Q000294:innervation; D004151:Dipeptides / Q000494:pharmacology; D006321:Heart / Q000187:drug effects / Q000502:physiology*; D006439:Hemodynamics / Q000187:drug effects; D007150:Immunohistochemistry; D066298:In Vitro Techniques; D007211:Indoles / Q000494:pharmacology; D008297:Male; D009206:Myocardium / Q000378:metabolism; D009479:Neuropeptides / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D010101:Oxygen Consumption; D051381:Rats; D013373:Substance P / Q000037:antagonists & inhibitors / Q000502:physiology; D016277:Ventricular Function, Left / Q000187:drug effects
chemical_list: D004151:Dipeptides; D007211:Indoles; D009479:Neuropeptides; C078949:FK 888; D013373:Substance P; D015740:Calcitonin Gene-Related Peptide; D000241:Adenosine; D002211:Capsaicin