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Sex Differences in Renal and Cardiovascular Function: Physiology and Pathophysiology

Effect of sex hormones on renal estrogen and angiotensin type 1 receptors in female and male rats

Departments of ¹Physiology and Biophysics and ²Medicine and ³Center for the Study of Sex Differences in Health, Aging and Disease, Georgetown University School of Medicine, Washington, DC

Submitted 6 June 2006 ; accepted in final form 19 September 2006

Although the mechanisms are not understood, evidence suggests that 17-estradiol (E₂) confers protection from cardiovascular and renal complications in many diseases. We have reported that E₂ decreases angiotensin type 1 receptors (AT₁Rs) in different tissues and hypothesize that E₂ exerts tonic inhibition on AT₁Rs, reducing effects of ANG II. This study determined the effects of E₂ and dihydrotestosterone (DHT) on cortical estrogen receptors (ERs) and glomerular AT₁R binding in rats. Animals underwent sham operation, ovariectomy (Ovx) or orchidectomy (Cas) and were treated (Ovx ± E₂; Cas ± DHT) for 3 wk. Cortical ER protein was 2.5 times greater, and ER was 80% less in females vs. males (P < 0.01). Glomerular AT₁R binding was lower in females than males [4,657 ± 838 vs. 7,457 ± 467 counts per minute (cpm), P < 0.01]. Ovx reduced ER protein by 50%, whereas E₂ increased ER expression after Ovx. The decrease in cortical ER in Ovx rats was associated with a significant increase in AT₁R binding (6,908 ± 609 cpm), and E₂ prevented this increase. There was no change in ER or AT₁R binding following Cas ± DHT (25 mg) treatment, although Cas did elevate cortical ER (P < 0.01). Interestingly, the high dose DHT (200 mg) elevated ER 150% above intact levels and profoundly decreased AT₁R binding (1,824 ± 705 cpm, P < 0.001 vs. intact male). This indicates that under normal conditions, glomerular AT₁R binding is significantly greater in male than female animals, which may be important in development of cardiovascular and renal disease in males. Furthermore, E₂ regulates ER and is inversely associated with glomerular AT₁R binding, supporting our hypothesis that E₂ tonically suppresses AT₁Rs and suggesting a potential mechanism for the protective effects of estrogen.

kidney; 17-estradiol; dihydrotestosterone; testosterone; ovariectomy; castration; angiotensin II

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