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In previous studies we have demonstrated that 3 and estrogen  receptor subtypes are present in human vascular endothelial cells and coupled to constitutive nitric oxide synthase (cNOS) stimulation. In the present report we demonstrate that internal thoracic artery (ITA) endothelia express a  opioid receptor mRNA transcript and exposure of these transcripts to increasing concentrations of 17 -estradiol significantly diminishes ITA  opioid receptor expression. Exposure of ITA endothelia to SNAP, a NO donor, also diminishes  opioid receptor gene expression, suggesting that NO mediates, in an L-NAME (N G nitro-L-arginine methyl ester) and tamoxifen sensitive manner, 17 -estradiol‟s down regulating action. ITA endothelia also express an estrogen  receptor subtype and, when treated with morphine, in an L-NAME and naloxone sensitive manner diminishes the  estrogen receptor‟s expression. This demonstrates an interactive receptor mediated process via NO for both signaling agents. Additionally, morphine and estrogen actions were examined for their ability to alter adhesion to ITA segments. This treatment resulted in a concentration dependent decrease in monocyte adherence to the vessels at 30 min. Exposure to both agents did not decrease monocyte adherence further. Exposure to L-NAME or either naloxone or tamoxifen, opiate and estrogen cell surface receptor inhibitors, respectively, blocked the decrease in monocyte adherence, demonstrating NO involvement and a specific receptor mediated process. In conclusion, this study demonstrates that an interactive receptor mediated process via NO for both signaling agents is present.

Estrogen and Morphine Modulate Their Own and the Other's Human Endothelial Receptor Expression via Nitric Oxide