Abstract P039: Testosterone Increases BP in Male SHR by Activating the Renin-angiotensin System: A Cautionary Tale for “Low T” Supplements
Testosterone supplements are widely prescribed for men in the US to improve overall quality of life by increasing libido and sexual performance and protecting against osteoporosis. Whether testosterone supplements affect CVD either positively or negatively is not clear since study results are controversial. Previously, we showed that chronic testosterone supplements cause hypertension in obese male Zucker rats but improves inflammation and metabolic syndrome symptoms. We also found that testosterone supplements in young male SHR further increase their BP, and that castration attenuates the hypertension. In the present study we followed up on these previous studies and tested the hypothesis that, because the SHR are lean, chronic testosterone supplements will increase lean body mass but increase the BP via a renin angiotensin system (RAS) mechanism. Male SHR were treated with testosterone (8 mg/10 mm silastic pellet implanted sc) or placebo (empty pellets sc), beginning at 12 weeks of age for 8 weeks. Fat mass and lean mass were measured by ECHO MRI. Contrary to our hypothesis, testosterone supplements had no effect on lean mass, but reduced fat mass by 49% (4.9±0.6 vs 2.5±0.4 %BW, p<0.05). Baseline mean arterial pressure (MAP by telemetry) was higher in testosterone supplemented rats than placebo controls (157±0.4 vs. 147±0.7 mmHg, p<0.05). Enalapril (200 mg/L) reduced MAP by 25% in testosterone group (157±0.4 vs 118±6 mmHg, p<0.05) and by 14% placebo rats (148±0.5 vs 127±5 mmHg, p<0.05). MAPs after enalapril were similar between placebo and testosterone-treated rats. These data suggest that the RAS contributes to the elevated BP in testosterone supplemented male SHR. The data also suggest that caution should be taken in prescribing hypertensive men with testosterone supplements. Supported by NIH-R01HL66072, PO1HL51971 (JFR), 14POST18640015 (ROM), EFF Endocrine Res Grant (LLY).
Author Disclosures: R.O. Maranon: None. L.L. Yanes Cardozo: None. C. Dalmasso: None. C.N. Patil: None. H. Zhang: None. A. Harris: None. J.F. Reckelhoff: None.
This research has received full or partial funding support from the American Heart Association, Greater Southeast Affiliate (Alabama, Florida, Georgia, Louisiana, Mississippi, Puerto Rico & Tennessee).
- © 2015 by American Heart Association, Inc.