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(Hypertension. 2009;53:324.)
© 2009 American Heart Association, Inc.

Original Articles Part 2

Contribution of Endothelin A Receptors in Endothelin 1–Dependent Natriuresis in Female Rats

From the Vascular Biology Center, Medical College of Georgia, Augusta.

Correspondence to David M. Pollock, Vascular Biology Center, Medical College of Georgia, 1459 Laney Walker Blvd, Augusta, GA 30912. E-mail dpollock{at}mcg.edu

Renal medullary endothelin B receptors contribute to blood pressure regulation by facilitating salt excretion. Premenopausal females have relatively less hypertension than males; therefore, we examined whether there is a sex difference in the natriuretic response to renal medullary infusion of endothelin peptides in the rat. All of the experiments were conducted in anesthetized wild-type (wt) or endothelin B–deficient (sl/sl) rats. Infusion of endothelin 1 (ET-1) significantly increased sodium excretion (U_NaV) in female, but not male, wt rats (U_NaV: 0.41±0.07 versus –0.04±0.06 µmol/min, respectively). The endothelin B receptor agonist sarafotoxin 6c produced similar increases in U_NaV in both male (0.58±0.15 µmol/min) and female (0.67±0.18 µmol/min) wt rats. Surprisingly, ET-1 markedly increased U_NaV in female (0.70±0.11 µmol/min) but not male sl/sl rats (0.00±0.05 µmol/min). ET-1 had no effect on medullary blood flow in females, although medullary blood flow was significantly reduced to a similar extent in males of both strains. These results suggest that the lack of a natriuretic response to ET-1 in male rats is because of reductions in medullary blood flow. Treatment with ABT-627, an endothelin A receptor antagonist, or N^G-propyl-L-arginine, an NO synthase 1 inhibitor, prevented the increase in U_NaV observed in female rats. Gonadectomy eliminated the sex difference in the U_NaV and medullary blood flow response to ET-1. These findings demonstrate that there is no sex difference in endothelin B–dependent natriuresis, and the endothelin A receptor contributes to ET-1–dependent natriuresis in female rats, an effect that requires NO synthase 1. These findings provide a possible mechanism for why premenopausal women are more resistant to salt-dependent hypertension.

Key Words: sex • endothelin 1 • sodium excretion • ET_AET_Bmedullary blood flow

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