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Am J Physiol Heart Circ Physiol 294: H1923-H1932, 2008. First published January 25, 2008; doi:10.1152/ajpheart.01221.2007
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Rho kinase is involved in Ca2+ entry of rat penile small arteries

Nuria Villalba,1,2 Edgaras Stankevicius,2 Ulf Simonsen,2 and Dolores Prieto1

1Departamento de Fisiología, Facultad de Farmacia, Universidad Complutense, Madrid, Spain; and 2Department of Pharmacology, Faculty of Health Sciences, University of Aarhus, Aarhus C, Denmark

Submitted 22 October 2007 ; accepted in final form 25 January 2008

Tonic physiological activity of RhoA/Rho kinase contributes to the maintenance of penile flaccidity through its involvement in the Ca2+ sensitization of erectile tissue smooth muscle. The present study hypothesized that Rho kinase is also involved in the modulation of Ca2+ entry induced by {alpha}1-adrenoceptor stimulation of penile arteries. Rat penile arteries were mounted in microvascular myographs for simultaneous measurements of intracellular Ca2+ ([Ca2+]i) and force. The Rho-kinase inhibitor Y-27632 markedly reduced norepinephrine-mediated electrically induced contractions and the increases in both [Ca2+]i and tension elicited by the {alpha}1-adrenoceptor agonist phenylephrine (Phe). In contrast, the protein kinase C (PKC) inhibitor Ro-31-8220 reduced tension without altering the Phe-induced increase in [Ca2+]i. In the presence of nifedipine, Y-27632 still inhibited the non-L-type Ca2+ signal and blunted Phe contraction. Y-27632 did not impair the capacitative Ca2+ entry evoked by store depletion with cyclopiazonic acid but largely reduced the Ba2+ influx stimulated by Phe in fura-2 AM-loaded arteries. The addition of Y-27632 to arteries depolarized with high KCl markedly reduced tension without changing [Ca2+]i. In {alpha}-toxin-permeabilized penile arteries stimulated with threshold Ca2+ concentrations, Y-27632 inhibited the sensitization induced by either guanosine 5'-O-(3-thiotriphosphate) (GTP{gamma}S) or Phe in the presence of GTP{gamma}S. However, Y-27632 failed to alter contractions induced by a maximal concentration of free Ca2+. These results suggest that Rho kinase, besides its contribution to the Ca2+ sensitization of the contractile proteins, is also involved in the regulation of Ca2+ entry through a nonselective cation channel activated by {alpha}1-adenoceptor stimulation in rat penile arteries.

penile arteries; calcium entry; nonselective cation channels; calcium sensitization



Address for reprint requests and other correspondence: D. Prieto, Dept. de Fisiología, Facultad de Farmacia, Univ. Complutense, 28040-Madrid, Spain (e-mail: dprieto{at}farm.ucm.es)




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[Abstract] [Full Text] [PDF]




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