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Participation of K+ Channels in the Endothelium-Dependent and Endothelium-Independent Components of the Relaxant Effect of Rosuvastatin in Rat Aortic Rings

Sección de Estudios de Posgrado e Investigación de la Escuela Superior de Medicina, I.P.N. Plan de San Luis y Díaz Mirón, Col. Casco de Sto. Tomas, skiold666{at}hotmail.com

Roberto Mendoza, MD

Sección de Estudios de Posgrado e Investigación de la Escuela Superior de Medicina, I.P.N. Plan de San Luis y Díaz Mirón, Col. Casco de Sto. Tomas

Guadalupe Cleva Villanueva, MD

Sección de Estudios de Posgrado e Investigación de la Escuela Superior de Medicina, I.P.N. Plan de San Luis y Díaz Mirón, Col. Casco de Sto. Tomas

Gustavo Martínez, MD

Laboratorios Astra Zéneca, México

Enrique F. Castillo, MD

Sección de Estudios de Posgrado e Investigación de la Escuela Superior de Medicina, I.P.N. Plan de San Luis y Díaz Mirón, Col. Casco de Sto. Tomas

Carlos Castillo, MD

Sección de Estudios de Posgrado e Investigación de la Escuela Superior de Medicina, I.P.N. Plan de San Luis y Díaz Mirón, Col. Casco de Sto. Tomas

Rosuvastatin was tested on rat aortic rings in the presence and absence of K⁺ channel blockers, mevalonic acid, and inhibitors of nitric oxide, prostaglandins, or endothelial-derived hyperpolarizing factor synthesis. The direct vascular effects of rosuvastatin were then evaluated by obtaining dose—response curves. Rosuvastatin relaxed aortic rings with and, to a lesser degree, without endothelium. Under both these conditions this effect was partially inhibited by L-NAME, tetraethylammonium, apamin + charybdotoxin (only administered together), or mevalonic acid. The combination of L-NAME with any of the other 3 treatments completely inhibited the effect of rosuvastatin, but indomethacin, clotrimazol, glibenclamide, charybdotoxin, or apamin alone had no effect. Therefore, the relaxation induced by rosuvastatin, even in the absence of endothelium, is partially related to 2 different mechanisms, one that is isoprenoid dependent and NO mediated and the other that is tied to the opening of Ca ²⁺-dependent K⁺ channels of the slow subfamily.

Key Words: aorta • rosuvastatin • endothelium-dependent relaxation • potassium channels

This version was published on September 1, 2008

Journal of Cardiovascular Pharmacology and Therapeutics, Vol. 13, No. 3, 207-213 (2008)
DOI: 10.1177/1074248408321716


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