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The study tested the hypothesis that human chorionic gonadotrophin (hCG) attenuates isolated vascular smooth muscle contractility and investigated the role of the vascular endothelium in hCG-induced altered responses of vascular smooth muscle. The contractile responses of isolated aortic rings from normal, hCG-treated, and estrogen-treated female virgin Wistar rats to phenylephrine, angiotensin II, KCl, and CaCl2 were compared. The effect of pretreatment with N-monomethyl-L-arginine (L-NMMA), methylene blue, indomethacin, calcium-free medium, and de-endothelialization on responses to phenylephrine of aortic rings from control and hCG-treated rats were also examined. Intraperitoneal administration of hCG caused attenuation of contractile responses of isolated aortic rings to all agents. The attenuated responses to phenylephrine were not reversed by de-endothelialization, or pretreatment of the rings with L-NMMA, methylene blue, or indomethacin. It was concluded that hCG attenuates vascular smooth muscle contractility. The effect is independent of the vascular endothelium, not agonist-specific, and appears to involve alterations of calcium availability.

Human chorionic gonadotrophin is an endothelium-independent inhibitor of rat aortic smooth muscle contractility