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Advances in Pharmacological Sciences
Volume 2010 (2010), Article ID 534184, 10 pages
http://dx.doi.org/10.1155/2010/534184
Research Article

Testosterone and Cholesterol Vasodilation of Rat Aorta Involves L-Type Calcium Channel Inhibition

1CICS—Centro de Investigação em Ciências da Saúde, Universidade da Beira Interior, Av. Infante D. Henrique, 6200-506 Covilhã, Portugal
2Centro Hospitalar da Cova da Beira E.P.E., Quinta do Alvito, 6200-251 Covilhã, Portugal

Received 8 November 2009; Revised 7 January 2010; Accepted 16 January 2010

Academic Editor: Masahiro Oike

Copyright © 2010 E. Álvarez et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Testosterone has rapid nongenomic vasodilator effects which could be involved in protective cardiovascular actions. Several authors suggested specific mechanisms to explain this effect, but this matter was not clarified yet. We studied the actions of testosterone and cholesterol on endothelium-denuded rat aorta and their effects on the L-type current ( ) and potassium current ( ). Testosterone (1–100  M) totally relaxed, in a rapid and concentration-dependent way, the aortic rings contracted by KCl or by ( )-Bay K8644 (BAY). Cholesterol also fully relaxed the contractions induced by KCl. None of the potassium channel antagonists tested (glibenclamide, tetraethylammonium and 4-aminopyridine) modified significantly the relaxant effect of testosterone. The antagonist of classic testosterone receptors, flutamide, did not modify the vasorelaxant effect of testosterone. Furthermore, testosterone and cholesterol inhibited either basal and BAY-stimulated in A7r5 cells and they have no effects on . In summary, our results demonstrate that cholesterol and testosterone relax rat aorta by inhibiting LTCC. This effect of testosterone is not mediated by the classic hormone receptor or by potassium channel activation. These results suggest that the vasodilator mechanism of cholesterol and testosterone is the same.