Abstract
A thorough understanding of the renal and cardiovascular adaptations to normal gestation is essential for proper diagnosis and management of hypertensive disorders and renal diseases during pregnancy. Here, we briefly review the renal hemodynamic changes of normal pregnancy. In addition, we present new findings and current concepts related to the underlying hormonal and molecular mechanisms. Finally, we speculate on the potential contribution of these insights from normal pregnancy to the pathogenesis of preeclampsia.
Notes
1The increases in GFR and ERPF that occur during rat gestation before the ovarian secretion of relaxin begins on gestational day 9 or during pseudopregnancy when circulating relaxin is undetectable are likely to be mediated by other, as yet, undefined mechanisms
2Although both pregnancy and relaxin administration to nonpregnant female rats produce renal vasodilation, hyperfiltration, and reduced myogenic reactivity of small renal arteries that is dependent upon NO, the urinary excretion of cGMP and NO metabolites is only increased during pregnancy. Ironically, the increased production of cGMP and NO metabolites that we observed during rat gestation, and which spurned our investigation of this vasodilatory pathway, may not be of vascular origin or of hemodynamic consequence(Danielson et al. Citation1999; Conrad and Vernier Citation1989; Conrad et al. Citation1993)