Possible Involvement of K+ Channel Opening to the Interleukin-1β-Induced Inhibition of Vascular Smooth Muscle Contraction

Journal of Veterinary Medical Science

Hideaki Karaki¹  Hiroshi Ozaki¹  Satoko Takizawa¹ 

[1] Department of Veterinary Pharmacology, Graduate School of Agriculture and Life Sciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-8657, Japan

关键词: interleukin-1β;    K+ channel;    relaxation;    vascular smooth muscle;   

DOI  :  10.1292/jvms.61.357

学科分类：兽医学

来源: Japanese Society of Veterinary Science

【 摘 要 】

References(15)Cited-By(7)We have previously shown that interleukin-1β relaxes vascular smooth muscle by the NO-dependent and independent mechanisms (Takizawa et al.: Eur. J. Pharmacol. 330: 143-150, 1997). In this study, we investigated the mechanism of NO-independent relaxation. Treatment of the rat aorta with interleukin-1β for 24 hr inhibited the high-K+ induced contraction by decreasing cytosolic Ca2+ level ([Ca2+]i). The relationship between [Ca2+]i and tension in intact muscle and the pCa-tension curves in permeabilized muscle suggested that Ca2+ sensitivity of contractile element was not changed after the interleukin-1β-treatment. After a treatment with interleukin-1β for 24 hr, contractile effects of phenylephrine (1 μM-10 μM) were markedly inhibited in the presence of L-NMMA (100 μM) applied to inhibit NO synthesis. A blocker of ATP-sensitive K+ channel, glibenclamide (1 μM), partially recovered the interleukin-1β-induced inhibition. In contrast, a blocker of Ca2+-activated K+ channel, charybdotoxin (0.1 μM), was ineffective. These results suggest that membrane hyperpolarization due to activation of ATP-sensitive K+ channels may partly be responsible for the NO-independent mechanism of interleukin-1β-induced inhibition of vascular smooth muscle contraction.

【 授权许可】

Unknown