Use of the rat model to study hCG/LH effects on uterine blood flow

Luteinizing hormone (LH) and human chorionic gonadotropin (hCG) share a common receptor. LH/hCG receptors, located in the vascular smooth muscle and endothelial cells of uterine blood vessels, are most numerous in smaller intramyometrial vessels and are cyclic in nature. There is a correlation between hCG levels and decreased uterine vascular resistance in humans, and in pseudopregnant rats, hCG decreases uterine blood flow. We found that systemic administration of hCG to cycling rats reduced uterine blood flow within 20 minutes on all days of the estrous cycle when flow was measured via the radioactive microsphere method. This effect was absent in ovariectomized rats. To determine the response to hCG at the microvascular level, we measured uterine arteriolar diameters in vivo via videomicroscopy after direct application or injection of hCG in rats on diestrus-1, diestrus-2, and proestrus. When hCG was suffused over the uterus (20 IU/60 mL), the uterine arterioles in diestrus (1 and 2) rats dilated but in proestrus rats were constricted. Neither response was altered in animals whose ovaries were removed 3 hours previously. An intraperitoneal injection of hCG (50 IU) caused uterine arteriolar constriction in diestrus-2 and proestrus animals but no change in diestrus-1. In ovariectomized rats, uterine arteriolar constriction following hCG injection was absent. Thus, the response of the uterine vasculature is not only cycle day dependent but also dependent on the route of administration. The effect of hCG on uterine blood flow in the rat may be a direct action of hCG, or it could be secondary to the release of other vasoactive substances known to be released by hCG. hCG might also alter blood flow by inducing angiogenesis.