[Adaptation to short-term stress exposure increases the activity ATP-sensitive potassium channels in the smooth muscle cells of coronary blood vessels].
The study was aimed at the effect of prior adaptation to short-term stress exposure on changes in K(ATP)-channel activity induced by severe stress and the dependence of the changes on the state of endothelium which plays important role in autoregulation of the coronary flow and myocardial contractility. Experiments were conducted on isolation hearts of female rats. At the first step of experiment, the heart was perfused by Krebs-Henseleit solution; at the second step, the heart was perfused with the same solution in which glibenclamide (1 microM), glibenclamide with saponin or N(omega)-nitro-L-arginine (60 microM) methyl ether was added. During the experiment, the perfusion pressure was stepwise elevated from 40 to 120 mm Hg with 20 mm intervals (coronary autoregulation). Adaptation to short-term stress prevented development of stress-specific myocardial hyperperfusion (increased volumetric velocity of coronary flow against the background of decreased myocardial contractility) and the reduction of coronary dilation reserve. In coronary vessels of adapted rats, as distinct from control rats, basal glibenclamide-sensitive functional activity of K(ATP)-channels depended on presence and functional activity of endotheliocytes; it was reduced in presence of endothelium and increased after de-endothelization or NO synthase inhibition. In all experimental groups, the increase in glibenclamide-sensitive functional activity of K(ATP)-channels induced by NO synthase inhibition more than twice as great as after the endothelium denudation. In adapted animals, stress did not decrease the functional activity of K(ATP)-channels and their activity slightly depended on presence of endotheliocytes. In addition, the elevation of their functional activity characteristic of adaptation and evident after endothelium removal has vanished. Therefore adaptation to short-term stress exposure is associated with a potential increase in basal activity of K(ATP)-channels which enhances the potency of vascular dilation system and may apparently reduce the risk of high vascular tone when such important local regulatory system as the NO system is damaged.
Lazuko
S S
SS
Solodkov
A P
AP
Manukhina
E B
EB
D000222:Adaptation, Physiological; D000818:Animals; D003331:Coronary Vessels / Q000502:physiology*; D004730:Endothelium, Vascular / Q000502:physiology; D005260:Female; D005905:Glyburide / Q000494:pharmacology; D066298:In Vitro Techniques; D015640:Ion Channel Gating; D009131:Muscle, Smooth, Vascular / Q000502:physiology*; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D012503:Saponins / Q000494:pharmacology; D013315:Stress, Psychological / Q000378:metabolism* / Q000503:physiopathology; D014662:Vasoconstrictor Agents / Q000494:pharmacology
D015221:Potassium Channels; D012503:Saponins; D014662:Vasoconstrictor Agents; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D005905:Glyburide; D019331:NG-Nitroarginine Methyl Ester