Mechanical responses of isolated dog cerebral arteries to reduction of external K, Na, and Cl.
Reduction of the extracellular potassium concentration ([K+]0) caused a significant contraction in helical strips of dog cerebral arteries, but only a slight contraction, or none, in peripheral (coronary, mesenteric, renal, and femoral) arteries. The cerebroarterial contraction was abolished by treatment with ouabain or by substitution of Li+ for Na+, and suppressed by exposure to Ca2+-free media or verapamil. When one-half of the NaCl of the bathing solution was substituted with choline chloride a moderate, sustained contraction was produced in cerebral and peripheral arteries. Ouabain potentiated this contraction, whereas exposure to Ca2+-free media abolished it. Substitution of Na propionate, NaI, or Na acetylglycinate for one-half of the NaCl elicited a marked, transient contraction in only the cerebral arteries. This contractile response was potentiated by ouabain and markedly attenuated by exposure to Ca2+-free media. It may thus be concluded that cerebroarterial contractions induced by a reduction in [K+]0 are due to inhibition of the electrogenic Na+ pump, which results in depolarization of smooth muscle cells. Substitution of Cl- with less permeant anions appears to produce cerebroarterial contraction in association with depolarization of smooth muscle cells.
D000818:Animals; D002536:Cerebral Arteries / Q000502:physiology*; D002712:Chlorides / Q000494:pharmacology*; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects*; D009130:Muscle, Smooth / Q000502:physiology; D011188:Potassium / Q000494:pharmacology*; D012964:Sodium / Q000494:pharmacology*
D002712:Chlorides; D012964:Sodium; D011188:Potassium