Is relaxin the “elusive” vasodilator of pregnancy?

Abstract

Among the most striking changes seen in biology are those associated with pregnancy. In particular, profound vasodilation of nonreproductive organs epitomizes the maternal cardiovascular adaptation to early gestation in women. Cardiac output, renal blood flow and glomerular filtration rate rise by 40 to 80%, while vascular resistances plummet and blood pressure declines modestly [reviewed in ref.1]. Global arterial compliance markedly increases, thus preserving the efficiency of ventricular and arterial coupling, as well as preventing excessive decline of diastolic blood pressure in the face of the marked fall in systemic vascular resistance [SVR; 2]. All of these alterations begin immediately after conception, peak by the end of the first or beginning of the second trimester, and persist throughout most of gestation. It is likely that the circulations of nonreproductive organs such as the kidney serve as “arteriovenous” shunts during early gestation, thereby reducing ventricular afterload which initiates the enormous increase in cardiac output, and subsequently, the expansion of plasma volume — maternal adaptations associated with healthy pregnancies. Furthermore, pressor response to administration of angiotensin II and vascular reactivity to infusion of norepinephrine become attenuated [1]. Insight into the mechanisms responsible for these vasodilatory phenomena may be particularly critical, because in preeclampsia, the attenuation of pressor responsiveness to angiotensin II, the reduced vascular reactivity to norepinephrine, as well as the systemic and renal vasodilation are compromised [1].