Testosterone Exacerbates Hypertension and Reduces Pressure-Natriuresis in Male Spontaneously Hypertensive Rats

TLDR

Investigate how testosterone influences blood pressure regulation and pressure‑natriuresis in male spontaneously hypertensive rats. Use intact, gonadectomized, and testosterone‑treated male and female rats over five weeks to compare blood pressure and pressure‑natriuresis responses. Testosterone raises systolic and mean arterial pressure in male SHR and ovariectomized females and blunts pressure‑natriuresis, indicating that male sex hormones aggravate hypertension in SHR.

Abstract

Studies were performed in intact male and female, gonadectomized male and female, and gonadectomized female rats given testosterone for 5 weeks to investigate the role played by testosterone in altered blood pressure control and pressure-natriuresis in male SHR. Serum testosterone levels reached a peak at 12 weeks of age in intact male SHR. Systolic blood pressure, measured weekly from 5 to 20 weeks of age, was similar between groups until 12 weeks of age when blood pressure became higher in males (195±3 mm Hg) than in females (168±3 mm Hg) or males castrated at 4 weeks (173±4 mm Hg). At 17 to 19 weeks direct measurement of arterial pressure in anesthetized rats confirmed that mean arterial pressure was higher in male (182±1 mm Hg) than in female (159±2 mm Hg) and castrated male SHR (159±2 mm Hg). In addition, testosterone (5 mg in Silastic pellets, SC for 5 weeks) administered to ovariectomized (ovx+T) females caused arterial pressure to increase by mm11% (175±2 mm Hg), which was significantly higher than in intact female, castrated male, or untreated ovariectomized (ovx) female SHR (158±2 mm Hg). Acute pressure-natriuresis was blunted in male SHR compared with females, castrated males, or ovx females, in which this relationship was similar. Pressure-natriuresis was also blunted in ovx+T females as found in intact male SHR. These data support the hypothesis that male sex hormones contribute to the exacerbation of hypertension in SHR by reducing pressure-natriuresis.