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(Circulation Research. 2000;87:112.)
© 2000 American Heart Association, Inc.

Cellular Biology

Inhibition by Protein Kinase C of the K_NDP Subtype of Vascular Smooth Muscle ATP-Sensitive Potassium Channel

William C. Cole, Todd Malcolm, Michael P. Walsh, Peter E. Light

From the Smooth Muscle Research Group, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada. Current address of P.E.L. is Department of Pharmacology, University of Alberta, Edmonton, AB, Canada.

Correspondence to Dr William C. Cole, Smooth Muscle Research Group, Faculty of Medicine, University of Calgary, 3330 Hospital Dr, NW, Calgary, Alberta, Canada, T2N 4N1. E-mail wcole{at}ucalgary.ca

Abstract—ATP-sensitive K⁺ channels (K_ATP) contribute to the regulation of tone in vascular smooth muscle cells. We determined the effects of protein kinase C (PKC) activation on the nucleoside diphosphate–activated (K_NDP) subtype of vascular smooth muscle K_ATP channel. Phorbol 12,13-dibutyrate (PdBu) and angiotensin II inhibited K_NDP activity of C-A patches of rabbit portal vein (PV) myocytes, but an inactive phorbol ester was without effect, and pretreatment with PKC inhibitor prevented the actions of PdBu. Constitutively active PKC inhibited K_NDP in I-O patches but was without effect in the presence of a specific peptide inhibitor of PKC. PdBu increased the duration of a long-lived interburst closed state but was without effect on burst duration or intraburst kinetics. PdBu treatment inhibited K_NDP, but not a 70-pS K_ATP channel of rat PV. The results indicate that the K_NDP subtype of vascular smooth muscle K_ATP channel is inhibited by activation of PKC. Control of K_NDP activity by intracellular signaling cascades involving PKC may, therefore, contribute to control of tone and arterial diameter by vasoconstrictors. (Circ Res. 2000;87:112-117.)

Key Words: vascular smooth muscle • potassium channel • protein kinase C

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