Activators of protein kinase C decrease Ca2+ spark frequency in smooth muscle cells from cerebral arteries

The American Journal of Physiology
A D BonevM T Nelson

Abstract

Local Ca2+ transients ("Ca2+ sparks") caused by the opening of one or the coordinated opening of a number of tightly clustered ryanodine-sensitive Ca(2+)-release (RyR) channels in the sarcoplasmic reticulum (SR) activate nearby Ca(2+)-dependent K+ (KCa) channels to cause an outward current [referred to as a "spontaneous transient outward current" (STOC)]. These KCa currents cause membrane potential hyperpolarization of arterial myocytes, which would lead to vasodilation through decreasing Ca2+ entry through voltage-dependent Ca2+ channels. Therefore, modulation of Ca2+ spark frequency should be a means to regulation of KCa channel currents and hence membrane potential. We examined the frequency modulation of Ca2+ sparks and STOCs by activation of protein kinase C (PKC). The PKC activators, phorbol 12-myristate 13-acetate (PMA; 10 nM) and 1,2-dioctanoyl-sn-glycerol (1 microM), decreased Ca2+ spark frequency by 72% and 60%, respectively, and PMA reduced STOC frequency by 83%. PMA also decreased STOC amplitude by 22%, which could be explained by an observed reduction (29%) in KCa channel open probability in the absence of Ca2+ sparks. The reduction in STOC frequency occurred in the presence of an inorganic blocker (Cd2+) of voltag...Continue Reading

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Citations

Jun 5, 1998·The American Journal of Physiology·J H JaggarM T Nelson
Jul 18, 2000·American Journal of Physiology. Cell Physiology·O BayguinovK M Sanders
Feb 15, 2001·American Journal of Physiology. Cell Physiology·O BayguinovK M Sanders
Aug 18, 2001·Journal of Applied Physiology·K M Sanders
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Jul 10, 2001·American Journal of Physiology. Cell Physiology·J H Jaggar
Nov 13, 2002·American Journal of Physiology. Heart and Circulatory Physiology·Thomas J HeppnerMark T Nelson
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