Cell surface estrogen receptors coupled to cNOS mediate immune and vascular tissue regulation: therapeutic implications.

The vast number of reports dealing with estrogen and its associated molecular signaling cascades deal with genomic processes. However, recently data is emerging that demonstrates that estrogen may also work via estrogen cell surface receptors. In this regard, we describe such receptors on human monocytes, granulocytes and vascular endothelial cells. It would appear that these receptors are coupled to constitutive nitric oxide synthase derived nitric oxide release via the stimulation of intracellular calcium transients. It is this cascade that has the ability to down regulate both immune and vascular cellular processes, i. e, adherence. Based on this, for example we surmise that in menopause an earlier initiation of estrogen therapy may be more beneficial so as to prevent a decrease in its cellular signaling and maintenance functions, at least with respect to NO-related events.