Abstract

There is now convincing experimental evidence documenting acute and transient actions of steroid hormones in the vasculature. Steroids can rapidly activate signalling cascades within endothelial and smooth muscle cells that seem to bypass the classical, genomic receptor. Activation of these signalling cascades, involving alterations in intracellular Ca2 and MAPK activity, leads to changes in membrane potential and/or Ca2 fluxes through L-type channels. In addition to stimulating NO production acutely in endothelial cells, chronic exposure to 17b-oestradiol may activate expression of eNOS via a genomic receptor(s).

Keywords: Rapid non genomic vasodilator actions, oestrogens, sex steroids, intracellular Ca2, MAPK activity, oestradiol, non genomic actions