title: Modulation of adrenergic coronary vasoconstriction via ATP-sensitive potassium channel.
abstract: We examined humoral and/or locally produced vasoactive factors involved in modulating sympathetic coronary vasoconstriction via the ATP-sensitive K (KATP) channel in 42 anesthetized dogs. Glibenclamide (30 micrograms.kg-1.min-1 ic or 0.6 mg.kg-1.min-1 left atrial injection) augmented coronary vascular resistance (CVR) at baseline and during cardiac sympathetic nerve stimulation (2-20 Hz), with a greater increase seen in the subepicardial region than in the subendocardial region both during beta-adrenergic receptor blockade and alpha- and beta-receptor blockade [P < 0.05 and P < 0.05 (n = 6 and 18 dogs), analysis of variance]. In contrast, pinacidil (10 micrograms.kg-1.min-1; n = 8 dogs) suppressed CVR. Glibenclamide enhanced CVR response to locally administered norepinephrine of 0.001-0.1 microgram.kg-1.min-1 (P < 0.05, analysis of covariance; n = 5 dogs) but did not enhance norepinephrine or neuropeptide Y overflow (n = 18 dogs). CVR was not modified by calcitonin gene-related peptide (CGRP) antagonist [CGRP-(8-37)], 8-phenyltheophylline, or N omega-nitro-L-arginine (n = 11 dogs). Thus sympathetic coronary vasoconstriction is modified by coronary vascular KATP channels with a transmural difference. However, CGRP, adenosine, and endothelial nitric oxide production are not involved in the modulation.
authors.affiliation: Department of Physiology, Tokai University School of Medicine, Kanagawa, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Mori
authors.forename: M
authors.initials: M
authors.lastname: Chujo
authors.forename: E
authors.initials: E
authors.lastname: Tanaka
authors.forename: A
authors.initials: A
authors.lastname: Yamakawa
authors.forename: Y
authors.initials: Y
authors.lastname: Shinozaki
authors.forename: M U
authors.initials: MU
authors.lastname: Mohamed
authors.forename: H
authors.initials: H
authors.lastname: Nakazawa
mesh_terms: D000241:Adenosine / Q000502:physiology; D000255:Adenosine Triphosphate / Q000502:physiology*; D000818:Animals; D015740:Calcitonin Gene-Related Peptide / Q000037:antagonists & inhibitors / Q000494:pharmacology / Q000502:physiology; D003326:Coronary Circulation / Q000187:drug effects / Q000502:physiology*; D004285:Dogs; D004558:Electric Stimulation; D005905:Glyburide / Q000494:pharmacology; D006146:Guanidines / Q000494:pharmacology; D009478:Neuropeptide Y / Q000494:pharmacology; D009569:Nitric Oxide / Q000502:physiology; D009638:Norepinephrine / Q000494:pharmacology; D010446:Peptide Fragments / Q000494:pharmacology; D020110:Pinacidil; D015221:Potassium Channels / Q000502:physiology*; D013564:Sympathetic Nervous System / Q000502:physiology; D013806:Theophylline / Q000031:analogs & derivatives / Q000494:pharmacology; D014655:Vascular Resistance / Q000187:drug effects / Q000502:physiology; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology*
chemical_list: D006146:Guanidines; D009478:Neuropeptide Y; D010446:Peptide Fragments; D015221:Potassium Channels; C058636:calcitonin gene-related peptide (8-37); D009569:Nitric Oxide; D020110:Pinacidil; D000255:Adenosine Triphosphate; D013806:Theophylline; C028322:8-phenyltheophylline; D015740:Calcitonin Gene-Related Peptide; D000241:Adenosine; D005905:Glyburide; D009638:Norepinephrine