Human chorionic gonadotropin dilates uterine and mesenteric resistance arteries in pregnant and nonpregnant rats.

Membrane receptors for human chorionic gonadotropin (hCG) are expressed in a variety of steroidogenic cells, and also in extragonadal tissues such as vessels of the female genital tract. We examined the possible contribution of hCG to the endocrine control of prearteriolar mesenteric and uterine vessels before and during pregnancy. Lumen diameters of isolated pressurized resistance arteries from Sprague-Dawley rats were measured using a video-electronic system. hCG produced marked and dose-dependent vasodilation. Uterine radial arteries were found to be highly sensitive to hCG (EC50 approximately =60 mU/ml) before and throughout gestation. Second-order mesenteric arteries from nonpregnant animals were even more sensitive (EC50=38 mU/ml), but, in these vessels, responsiveness to hCG was significantly attenuated by the pregnant state. Mechanical removal of the vascular endothelium did not reduce the degree of vasodilation mediated by hCG. The expression of hCG receptor mRNA in intact vessels could be demonstrated using reverse transcriptase polymerase chain reaction (RT-PCR). hCG appears to be an important embryonic signal, which could trigger adaptive cardiovascular changes in early pregnancy, simultaneously preserving a sufficient utero-placental perfusion during the entire gestation period by an endothelium-independent mechanism.