Synthesis and evaluation of the cardiovascular effects of two, membrane impermeant, macromolecular complexes of dextran-testosterone.

The incidence of cardiovascular disease is greater in men than in premenopausal women. Testosterone has been considered a significant risk factor for cardiovascular disease, but testosterone's mechanism of action and its cellular site of action are still not clear. However, it is likely that non-genomic extracellular effects of the hormone are involved.

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.