Role of Adrenal Mineralocorticoid in Volume Homeostasis and Pregnancy Performance in the Rat

Abstract

Because of disagreement regarding the importance of maternal adrenal mineralocorticoid in gestational volume homeostasis and reproductive performance, we studied pregnant rats consuming standard or moderately sodium-restricted diets (22 or 2.2 mEq/100 gm), each subjected on gestational day 5 to SHAM surgery (SHAM) or adrenalectomy (ADNX), the latter combined with corticosterone replacement. Some animals were instrumented with chronic vascular catheters to measure plasma volume and mean arterial pressure (MAP) responses to captopril. We found that neither absolute plasma volume nor hematocrit was significantly altered by adrenalectomy in animals on either standard or sodium-restricted diets. However, P_osmol, 9-10 mosmol/kg lower in SHAM pregnant than virgin controls, was 16-22 mosmol/kg below nonpregnant levels in ADNX dams. Despite this hypotonicity, plasma vasopressin (AVP) was not suppressed, suggesting hemodynamic stimulation of AVP secretion. Basal MAP was 105 ± 3 mm Hg and 100 ± 2 mm Hg in SHAM pregnant rats on normal and sodium-restricted diets, respectively, 114 ± 2 mm Hg in SHAM operated virgins, and 87 ± 4 mm Hg and 92 ± 5 mm Hg in pregnant ADNX on standard and sodium-restricted diets, respectively. Following captopril, MAP decreased ± 5% in SHAM gravid and virgin rats, but declined ± 20% in ADNX dams, indicating that blood pressure was highly angiotensin II (Ang II) dependent. Plasma aldosterone was greater in SHAM pregnant rats on standard chow (50 ± 13 ng/dl) than similarly treated virgins (27 ± 17 ng/dl) (P <0.02), but levels were barely detectable in ADNX pregnant groups. Adrenalectomized dams on both standard and low-sodium chow had significantly (P <0.001) smaller litters (± 4 pups) than did SHAM gravid animals on either diet (± 8 pups). We conclude that mineralocorticoid of adrenal origin plays an important role in regulation of “effective” intravascular volume and reproductive performance during normal rat pregnancy. It also appears that insufficient fetal aldosterone enters the maternal circulation to maintain physiologic levels.