Originally isolated by Hisaw and colleagues in 1926, relaxin was named for its capacity to soften the pubic syphysis. Produced primarily by the corpus luteum in both pregnant and nonpregnant women, relaxin peaks during the luteal phase of the menstrual cycle, declines in the absence of pregnancy, and rises again early in gestation under the stimulus of human chorionic gonaotrophin. During pregnancy, additional relaxin is produced by the chorion and the decidua. Gesta-tional functions of relaxin include softening the cervix, relaxing the uterine musculature, and enhancing endometrial angiogenesis. As a modulator of the cardiovascular changes of pregnancy, relaxin is both a potent systemic and renal vasodilator. Increased vascular gela-tinase activity and activation of the endothelin B receptor-nitric oxide pathway help mediate the vasodilatory effects of relaxin.
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