Increased Myogenic Tone and Diminished Responsiveness to ATP-Sensitive K + Channel Openers in Cerebral Arteries From Diabetic Rats

吡那地尔 内科学 脑动脉 超极化(物理学) 内分泌学 血管收缩 硝普钠 医学 收缩 克罗马卡林 格列本脲 糖尿病 循环系统 心脏病学 化学 一氧化氮 核磁共振波谱 有机化学
作者
Paul Zimmermann,Harm J. Knot,Andrá S. Stevenson,Mark T. Nelson
出处
期刊:Circulation Research [Lippincott Williams & Wilkins]
卷期号:81 (6): 996-1004 被引量:128
标识
DOI:10.1161/01.res.81.6.996
摘要

Abstract Diabetes mellitus has profound adverse effects on vascular and, in particular, endothelial function. Although pressure-induced constriction (“myogenic tone”) is a major contributor to the regulation of blood flow, little is known about the effects of diabetes on this response. Diabetes has been shown to diminish the dilation of cerebral arteries to synthetic ATP-sensitive K + (K ATP ) channel openers. In this study, we explored the effects of diabetes induced in rats by streptozotocin on cerebral artery (250 to 300 μm) myogenic tone and on vasodilations to the synthetic K ATP channel openers pinacidil and levcromakalim. Elevation of intravascular pressure caused a graded membrane potential depolarization and constriction, which was greater in arteries from diabetic rats compared with normal rats (at 60 mm Hg, 5 mV more depolarized and 22 μm more constricted). Pressurized arteries (at 60 mm Hg) from diabetic rats were 5- to 15-fold less sensitive to pinacidil and levcromakalim than were control arteries (EC 50 values for pinacidil and levcromakalim were 1.4 and 0.6 μmol/L, respectively, in diabetic animals and 0.3 and 0.04, respectively, in control animals; P <.05). Removal of the endothelium or addition of a NO synthase inhibitor, N G -nitro- l -arginine (LNNA), in control arteries decreased the sensitivity to K ATP channel openers and depolarized and constricted control arteries to levels similar to those observed in arteries from diabetic animals. Sodium nitroprusside caused a membrane potential hyperpolarization and enhanced the response to pinacidil in arteries from diabetic animals. Removal of the endothelium or LNNA had little effect on the apparent K ATP channel opener sensitivity, the membrane potential, and pressure-induced constrictions of arteries from diabetic animals. The results are consistent with the hypothesis that this type of diabetes leads to a decrease in tonic NO release from the endothelium, which in turn causes membrane potential depolarization and vasoconstriction, resulting in a diminished response to K ATP channel openers.
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