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Vasoconstrictors inhibit ATP-sensitive K+ channels in arterial smooth muscle through protein kinase C.
Bonev A, Nelson MT
Journal of General Physiology. 1996;108( 4):315-23.
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Abstract
The effects of vasoconstrictor-receptor (neuropeptide Y, alpha-adrenergic, serotonergic, histaminergic) stimulation on currents through ATP-sensitive potassium (KATP) channels in arterial smooth muscle cells were examined. Whole-cell KATP currents, activated by the synthetic KATP channel opener pinacidil or by the endogenous vasodilator, calcitonin gene-related peptide, which acts through protein kinase A, were measured in smooth muscle cells isolated from mesenteric arteries of rabbit. Stimulation of NPY-, alpha 1-, serotonin (5-HT2)-, and histamine (H1)-receptors inhibited KATP currents by 40-56%. The signal transduction pathway that links these receptors to KATP channels was investigated. An inhibitor of phospholipase C (D609) and of protein kinase C (GF 109203X) reduced the inhibitory effect of these vasoconstrictors on KATP currents from 40-56% to 11-23%. Activators of protein kinase C, a diacylglycerol analogue and phorbol 12-myristate 13-acetate (PMA), inhibited KATP currents by 87.3 and 84.2%, respectively. KATP currents, activated by calcitonin gene-related peptide, were also inhibited (47-87%) by serotonin, phenylephrine, and PMA. We propose that KATP channels in these arterial myocytes are subject to dual modulation by protein kinase C (inhibition) and protein kinase A (activation).
Keyword(s)
Animals; Electric Conductivity; Enzyme Activation; Potassium Channel Blockers; Rabbits; cytology: Mesenteric Arteries; drug effects: Potassium Channels; metabolism: Muscle, Smooth, Vascular; metabolism: Protein Kinase C; pharmacology: Adenosine Triphosphate; pharmacology: Calcitonin Gene-Related Peptide; pharmacology: Serotonin Antagonists; pharmacology: Vasoconstrictor Agents