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Am J Physiol Heart Circ Physiol 282: H457-H465, 2002; doi:10.1152/ajpheart.00546.2001
0363-6135/02 $5.00
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Vol. 282, Issue 2, H457-H465, February 2002

Altered PYK2 phosphorylation by ANG II in hypertensive vascular smooth muscle

Petra Rocic1, Tina M. Griffin2, Chastity N. McRae1, and Pamela A. Lucchesi1

1 Department of Physiology and Biophysics, University of Alabama at Birmingham, Birmingham, Alabama 35294; and 2 Cardiovascular Institute, Stritch School of Medicine, Loyola University, Maywood, Illinois 60153

10.1152/ajpheart 00546.2001.---Vascular smooth muscle cells (VSMC) from spontaneously hypertensive rats (SHR) exhibit increased cell growth compared with normotensive Wistar-Kyoto rats (WKY). ANG II stimulates growth via Gq-protein-coupled signaling that involves changes in cytosolic intracellular Ca2+ concentration ([Ca2+]i) and activation of protein kinase C (PKC) and mitogen-activated protein kinases. This study examines the role of the proline-rich tyrosine kinase 2 (PYK2) in hypertensive VSMC. Basal PYK2 phosphorylation in SHR VSMC was increased compared with WKY (0.44 ± 0.02 vs. 0.20 ± 0.02-fold). ANG II-induced activation of PYK2 in SHR VSMC was of greater magnitude (2.2 ± 0.2-fold in SHR; 1.4 ± 0.1-fold in WKY) and occurred more rapidly (peak activation at 2 min in SHR vs. 5 min in WKY). This effect was blocked by pretreatment with the [Ca2+]i chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid or the PKC inhibitor chelerythrine. Basal and ANG II-stimulated c-Fos expression was increased in SHR versus WKY VSMC. PYK2 downregulation with antisense oligonucleotides blocked ANG II-induced c-Fos expression. Increased PYK2 activation may be altered signaling cascades that regulate cell growth in hypertensive VSMC.

mitogen-activated protein kinase; spontaneously hypertensive rats; protein kinase C; calcium; c-Fos


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