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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.

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

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