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This Article Full Text Full Text (PDF) All Versions of this Article: 294/4/H1923    most recent 01221.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Villalba, N. Articles by Prieto, D. Search for Related Content PubMed PubMed Citation Articles by Villalba, N. Articles by Prieto, D.

Rho kinase is involved in Ca²⁺ entry of rat penile small arteries

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 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 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 -toxin-permeabilized penile arteries stimulated with threshold Ca²⁺ concentrations, Y-27632 inhibited the sensitization induced by either guanosine 5'-O-(3-thiotriphosphate) (GTPS) or Phe in the presence of GTPS. 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 ₁-adenoceptor stimulation in rat penile arteries.

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