AJP - Heart and Circulatory Physiology, Vol 264, Issue 2 547-H552, Copyright © 1993 by American Physiological Society

ARTICLES

alpha-Adrenergic augmentation of myogenic response in rat arterioles: role of protein kinase C

J. Watanabe, M. Keitoku, K. Hangai, A. Karibe and T. Takishima
First Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.

We tested the hypothesis that protein kinase C (PKC) activation plays a major role in alpha-adrenergic augmentation of the myogenic response in rat isolated arterioles. Lumen diameter measured was with a video-monitored microscopic system. Lumen diameter did not change (131 +/- 5 vs. 126 +/- 6 microns) despite an increase in lumen pressure from 40 to 100 mmHg. Phenylephrine (Phe; 3 x 10(-7) M) augmented the myogenic response, since lumen diameter decreased significantly from 117 +/- 8 to 101 +/- 8 microns. High potassium (40 mM) failed to augment the myogenic response, while constricting the vessels to nearly the same extent as did Phe. PKC inhibitors 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine dihydrochloride (H-7, 5 x 10(-5) M, n = 7) and staurosporine (3 x 10(-9) M, n = 7) abolished the Phe-induced augmentation. H-7 and staurosporine depressed the myogenic response even without Phe. PKC activators phorbol 12,13-dibutyrate (3 x 10(-9) M; n = 7) and 4 beta-phorbol 12-myristate 13-acetate (6 x 10(-8) M; n = 6) constricted the vessels by 11 +/- 2 and 18 +/- 3%, respectively. However, PKC activators failed to augment the myogenic response. These results suggest that PKC activation does not play a major role in alpha-adrenergic augmentation of the myogenic response in rat skeletal arterioles.

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