The alterations of vascular smooth muscle reactivity in vitro by human chorionic gonadotrophin

The study tests the hypothesis that human chorionic gonadotrophin (hCG) alt ers vascular smooth muscle reactivity by examining the effect of hCG admini stration on the contractility and relaxation of isolated vascular smooth mu scle. Aortic rings from rats pre-treated with intraperitoneal administratio n of 5,000 I.U of hCG and control animals were contracted to phenylephrine, angiotensin II, CaCl2 and KCl. The experiments with phenylephrine were rep eated with rings that were either de-endothelialized, incubated with L-NMMA , or incubated with calcium ionophore A23187. Aortic rings precontracted wi th phenylephrine were relaxed to acetylcholine (endothelium-dependent), sod ium nitroprusside, hydralazine (endothelium-independent) or in the presence of A23187. The contractile responses of aortic rings from hCG-treated anim als to phenylephrine, angiotensin II, CaCl2 and KCl were significantly atte nuated. This effect was not reversed by pre-treatment with L-NMMA or by de- endothelialisation. In aortic rings from hCG-treated animals, there was alm ost total inhibition of acetylcholine-induced relaxation, but unaltered rel axation responses to sodium nitroprusside and hydralazine. The inhibitory e ffects of hCG-treatment on both the contraction and relaxation responses we re either fully or partially reversed in the presence of calcium ionophore A23187. These observations suggest that hCG attenuates both contractile and endothelium-dependent relaxation responses by a mechanism which involves i nhibition of extracellular calcium ion influx and may indicate a new role f or the hormone in the altered vascular responses of both normal and abnorma l pregnancies.