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(Circulation Research. 1995;76:269-275.)
© 1995 American Heart Association, Inc.

Articles

Role of Extracellular and Intracellular Acidosis for Hypercapnia-Induced Inhibition of Tension of Isolated Rat Cerebral Arteries

Rong Tian, Pia Vogel, Niels A. Lassen, Michael J. Mulvany, Frederik Andreasen, Christian Aalkjær

From the Department of Pharmacology, University of Aarhus (Denmark), and the Department of Clinical Physiology (N.A.L.), Bispebjerg Hospital, Copenhagen, Denmark.

Correspondence to Dr Christian Aalkjær, Department of Pharmacology, University of Aarhus, 8000 Aarhus C, Denmark.

Abstract The importance of smooth muscle cell pH_i and pH_o for the hypercapnic vasodilation of rat cerebral arteries was evaluated in vitro. Vessel segments were mounted in a myograph for isometric tension recording; pH_i was measured by loading the smooth muscle cells with the fluorescent dye BCECF, and pH_o was measured with a glass electrode. In all studies, Ca²⁺-dependent basal tension (in the absence of any agonist) and tension in the presence of arginine vasopressin were investigated. Control solution was physiological saline bubbled with 5% CO₂ and containing 25 mmol/L HCO₃^- (pH 7.45 to 7.50). Induction of hypercapnic acidosis (10% CO₂) or normocapnic acidosis (15 mmol/L HCO₃^-) caused significant inhibition of smooth muscle tension, and both conditions reduced pH_i as well as pH_o. N-Nitro-L-arginine significantly inhibited the relaxation to hypercapnic acidosis but had no significant effect on relaxation to normocapnic acidosis. Predominant extracellular acidosis, induced by reducing [HCO₃^-] from 25 to 9 mmol/L and CO₂ from 5% to 2.5%, also caused inhibition of tension in steady state. By contrast, predominant intracellular acidosis, induced by increasing [HCO₃^-] from 25 to 65 mmol/L and CO₂ from 5% to 15%, induced a small increase of basal tension and a small decrease of tension in the presence of arginine vasopressin. The responses to predominant intracellular or extracellular acidosis were qualitatively similar in the presence and absence of endothelium and in the presence and absence of N-nitro-L-arginine. It is concluded that the extracellular acidosis and not smooth muscle intracellular acidosis is responsible for the relaxation to hypercapnic acidosis.

Key Words: cerebral arteries • pH • hypercapnia • nitric oxide

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