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Am J Physiol Cell Physiol 281: C17-C23, 2001;
0363-6143/01 $5.00
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Vol. 281, Issue 1, C17-C23, July 2001

ANG II-mediated inhibition of neuronal delayed rectifier K+ current: role of protein kinase C-alpha

Sheng-Jun Pan, Mingyan Zhu, Mohan K. Raizada, Colin Sumners, and Craig H. Gelband

Department of Physiology, College of Medicine, and McKnight Brain Institute, University of Florida, Gainesville, Florida 32610

It was previously determined that ANG II and phorbol esters inhibit Kv current in neurons cultured from newborn rat hypothalamus and brain stem in a protein kinase C (PKC)- and Ca2+-dependent manner. Here, we have further defined this signaling pathway by investigating the roles of "physiological" activators of PKC and different PKC isozymes. The cell-permeable PKC activators, diacylglycerol (DAG) analogs 1,2-dioctanoyl-sn-glycerol (1 µmol/l, n = 7) and 1-oleoyl-2-acetyl-sn-glycerol (1 µmol/l, n = 6), mimicked the effect of ANG II and inhibited Kv current. These effects were abolished by the PKC inhibitor chelerythrine (1 µmol/l, n = 5) or by chelation of internal Ca2+ (n = 8). PKC antisense (AS) oligodeoxynucleotides (2 µmol/l) against Ca2+-dependent PKC isoforms were applied to the neurons to manipulate the endogenous levels of PKC. PKC-alpha -AS (n = 4) treatment abolished the inhibitory effects of ANG II and 1-oleoyl-2-acetyl-sn-glycerol on Kv current, whereas PKC-beta -AS (n = 4) and PKC-gamma -AS (n = 4) did not. These results suggest that the angiotensin type 1 receptor-mediated effects of ANG II on neuronal Kv current involve activation of PKC-alpha .

antisense; calcium; angiotensin type 1 receptor


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