Acidosis-induced coronary arteriolar dilation is mediated by ATP-sensitive potassium channels in vascular smooth muscle

Circulation Research
H Ishizaka, L Kuo

Abstract

Although a decrease in extravascular pH has been suggested to be involved in coronary flow regulations during hypoxia, ischemia, and increased metabolic demand of the heart, its vasomotor control mechanism has not been elucidated. To examine the effect of acidosis of vasomotor tone, porcine coronary arterioles (40 to 110 microns) were isolated, cannulated, and pressurized to 60 cm H2O intraluminal pressure without flow for in vitro study. Acidosis (pH 7.4 to 7.0) was produced by adding HCl to the extravascular solution. The involvement of potassium channels in the vasomotor response to acidosis was evaluated by using BaCl2 (100 mumol/L, nonspecific potassium channel inhibitor), glibenclamide (5 mumol/L, ATP-sensitive potassium channel inhibitor), and iberiotoxin (100 nmol/L, calcium-activated potassium channel inhibitor). To determine whether endothelial hyperpolarization contributes to the acidosis-induced dilation, the pH-diameter relation of the vessel was examined under a high intraluminal concentration of KCl (40 mmol/L). The involvement of nitric oxide and prostaglandins was assessed by using NG-monomethyl-L-arginine (L-NMMA, 10 mumol/L) and indomethacin (10 mumol/L), respectively. To evaluate the role of endothelium in t...Continue Reading

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