The study tests the hypothesis that human chorionic gonadotrophin (hCG) alters vascular smooth muscle reactivity by examining the effect of hCG administration on the contractility and relaxation of isolated vascular smooth muscle. Aortic rings from rats pre-treated with intraperitoneal administration of 5,000 I.U of hCG and control animals were contracted to phenylephrine, angiotensin II, CaCl2 and KCl. The experiments with phenylephrine were repeated with rings that were either de-endothelialized, incubated with L-NMMA, or incubated with calcium ionophore A23187. Aortic rings pre-contracted with phenylephrine were relaxed to acetylcholine (endothelium-dependent), sodium nitroprusside, hydralazine (endothelium-independent) or in the presence of A23187. The contractile responses of aortic rings from hCG-treated animals to phenylephrine, angiotensin II, CaCl, and KCl were significantly attenuated. This effect was not reversed by pre-treatment with L-NMMA or by de-endothelialisation. In aortic rings from hCG-treated animals, there was almost total inhibition of acetylcholine-induced relaxation, but unaltered relaxation responses to sodium nitroprusside and hydralazine. The inhibitory effects of hCG-treatment on both the contraction and relaxation responses were 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 inhibition of extracellular calcium ion influx and may indicate a new role for the hormone in the altered vascular responses of both normal and abnormal pregnancies.
- Vascular smooth muscle
ASJC Scopus subject areas