RACIAL EFFECTS ON ESTROGEN MODULATION OF SODIUM AND BLOOD PRESSURE REGULATION.

Abstract

PURPOSE: To determine racial differences in the effect of estrogen on sodium regulation and blood pressure (BP) in young women. METHODS: We used a gonadotropin releasing-hormone (GnRH) analogue, leuprolide acetate, to suppress endogenous estrogen and progesterone in five black (B, age 27 ± 1 yr) and four white (W, age 24 ± 1 yr) women. Subjects received the GnRH analog alone for four weeks, followed by GnRH analog plus estrogen for one week. Under both hormonal conditions, we measured BP, sodium regulation hormones and body fluid responses to 3% NaCl infusion (HSI, 120 min, 0.1 ml/min/kg BW) followed by drinking (30 min, 15 ml/kg BW) and 90 min of recovery. RESULTS: Plasma [E2] increased from 25 ± 11 to 254 ± 70 pg/ml in B and from 37 ± 28 to 207 ± 64 pg/ml in W with hormone treatment while [P4] remained constant (0.4 ± 0.0 to 0.3 ± 0.0 ng/ml in B and 1.7 ± 1 to 2.0 ± 1 ng/ml in W). There were no baseline racial differences in PRA, plasma [ALD] or [ANP] during GnRH-alone or during estrogen treatment. Estrogen administration caused an increase in [ALD] in W (61.9 ± 22.1 to 103.3 ± 12.9 pg/ml, P < 0.05) but not in B (49.6 ± 7.7 to 59.4 ± 20.9 pg/ml), and the greater [ALD] persisted throughout HSI and recovery in W. In both groups, systolic blood pressure (SBP) was reduced at baseline during estrogen treatment (128 ± 4 to 122 ± 6 and 128 ± 5 to 123 ± 5 mm Hg, in B and W, respectively). During GnRH-alone, SBP was increased at 120 min of HSI in B (to 131 ± 6 mm Hg) and W (to 131 ± 4 mm Hg), but this increase occurred only in B during estrogen treatment (to 131 ± 4 and to 122 ± 5 mm Hg at 120 min of HSI, in B and W respectively). Neither renal sodium excretion nor body water balance was affected by estrogen in B or W. CONCLUSION: The attenuated BP response to HSI in W despite similar sodium excretion suggests estrogen may induce a shift in the pressure-natriuresis curve in white, but not black women. Further, this shift was associated with a reduction in ALD actions on distal tubule sodium regulation. NIH RO 1 HL62240-01A1.