[Relevance of L-type calcium channels for the non-genomic effects of estradiol and aldosterone upon contractile activity in isolated arteries].

2011 
Abstract Non-genomic vascular effects of steroids are incompletely understood, despite progress made regarding some aspects, such as the mechanism of endothelium-dependent relaxation by estrogens. To investigate the involvement of certain mechanisms in the rapid, non-genomic effects of estradiol (EST) and aldosterone (ALD) on endothelium-dependent and -independent vasomotor responses. Isometric myography of rings from aorta, mesenteric arch, and first order mesenteric branches isolated from male Wistar rats was used. We found that L-type calcium channels (Cav1.2) are important for endothelium-independent relaxation induced by EST, while ALD reduces the involvement of Cav1.2 in phenylephrine-induced contraction and potentates both NO- and EDHF-mediated endothelium-dependent relaxation. To further examine the relevance of Cav1.2 for the vascular effects of EST and ALD, we were using rings with and without functional endothelium, precontracted by direct activation of Cav1.2 (Bay K 8644), high extracellular K+, phenylephrine, and under complete Cav1.2 block (nifedipine). Data suggest that EST, which directly inhibits Cav1.2 in transfected HEK cells, uses mainly this path to induce endothelium-independent relaxation, and that ALD may induce a rightward shift in the voltage-dependence of Cav1.2.
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