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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

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