Testosterone inhibits bradykinin-induced intracellular calcium kinetics in rat aortic endothelial cells in culture.

Sex steroids have been associated with cardiovascular diseases and the modification of the risk of coronary artery disease (CAD). We cultured aortic endothelial cells from young adult male rats and loaded them with Fura 2 in order to evaluate the direct effects of testosterone on endothelial cells and the probable regulation of bradykinin-induced effects on intracellular calcium ([Ca(2+)](i)) kinetics, effects that are mediated through an increase in intracellular [IP(3)], which in turn stimulates the rapid release of Ca(2+) from ER stores. Our results show that testosterone had no direct effects on [Ca(2+)](i) kinetics, but did block bradykinin-induced increases in intracellular calcium concentration in endothelial cells. This effect was concentration-dependent; the steroid was applied only 30 s before bradykinin application and thus, the effect can be considered nongenomic in origin. Membrane localization of a putative androgen receptor in endothelial cells could be responsible for this effect. In summary, testosterone can modulate the effects induced by activation of membrane-bound bradykinin receptors.