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2, which corroborates one of the earliest reports of GFR measured in the first trimester by the 24-h endogenous creatinine clearance, as shown in Fig. This dramatic rise in RPF and GFR during early pregnancy is exemplified by the meticulous investigation of Chapman et al. RPF and GFR increase by 40–65 and 50–85%, respectively, during human pregnancy (reviewed in Refs. Renal vasodilation underlies the massive increase in effective renal plasma flow (ERPF) and glomerular filtration rate (GFR) during early gestation, as measured by the renal clearances of para-aminohippurate and inulin, respectively. ↓Myogenic Constriction, inhibition of myogenic constriction of small renal and mesenteric arteries harvested from gravid rats. SVR, systemic vascular resistance CO, cardiac output AC, arterial compliance RVR, renal vascular resistance RPF, renal plasma flow GFR, glomerular filtration rate P osm, plasma osmolality. Maternal circulatory and osmoregulatory adaptations to pregnancy in women are recapitulated in gravid rats. 1, the systemic circulatory adaptations of pregnancy in women have been modeled in the conscious gravid rat, including reduction in SVR and increases in CO and global arterial compliance ( 84, 176), thus affording the opportunity to explore potential hormonal and molecular mechanisms, as described below. The anticipatory nature of these gestational adaptations in the maternal circulation is underscored by the difference in arterial-mixed venous oxygen content, which narrows in early pregnancy, indicating that oxygen supply exceeds demands ( 10, 84, 156). Thus, these circulatory changes are apparently preparatory events in anticipation of the rapid growth phase of the fetus and placenta in the second half of gestation, when oxygen and nutrient demands accelerate, rising exponentially. Although counterintuitive, this metamorphosis of the maternal circulation is virtually complete by the end of the first or beginning of the second trimester, when fetal crown rump length and placental diameter are only ∼6 cm each ( 15) and uterine blood flow is ∼0.25 l/min (cf. The fall in SVR is nearly offset by the rise in CO hence, mean arterial pressure (MAP) declines, but only modestly, by 5–10 mmHg ( 23, 38, 163). Vasodilation of nonreproductive organs like the kidneys accounts mostly for the early gestational fall in SVR and rise in CO. Consequently, there is a precipitous and profound decline in systemic vascular resistance (SVR) that in turn abets a reciprocal increase in cardiac output (CO) of ∼40% or 2 l/min lasting throughout pregnancy ( 23, 163). Marked vasodilation of the maternal circulation occurs in the first trimester of human pregnancy. Renal Plasma Flow and Glomerular Filtration in Normal Pregnancy So far, one candidate to emerge is RLN and its potential therapeutic use in heart failure. Another goal has been to apply knowledge gained from investigating circulatory adaptations in pregnancy toward identifying and developing novel therapeutic strategies for renal and cardiovascular disease in the nonpregnant population. Last, potential clinical ramifications include RLN replacement in women conceiving with donor eggs and its therapeutic use in PE. Additional pathogenic factors are discussed. Elevated level of circulating soluble vascular endothelial growth factor receptor-1 arising from the placenta is implicated in the hypertension and disruption of glomerular fenestrae and barrier function, the former causing reduced K f and the latter proteinuria. In preeclampsia (PE), maternal systemic and renal vasoconstriction leads to hypertension and modest reduction in GFR exceeding that of RPF. Although RLN exerts both rapid (minutes) and sustained (hours to days) vasodilatory actions through different molecular mechanisms, a final common pathway is endothelial nitric oxide. Systemic and renal vasodilation are compromised in midterm pregnant rats by neutralization or elimination of circulating RLN and in women conceiving with donor eggs who lack a corpus luteum and circulating RLN. Administration of the corpus luteal hormone relaxin (RLN) to nonpregnant rats and humans elicits vasodilatory changes like those of pregnancy. Comparable circulatory adaptations are observed in conscious gravid rats. The kidneys participate in this vasodilatory response resulting in marked increases in renal plasma flow (RPF) and glomerular filtration rate (GFR). During the first trimester of human pregnancy, the maternal systemic circulation undergoes remarkable vasodilation.

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