Ganten U, Schröder G, Witt M, Zimmermann F, Ganten D, Stock G
Department of Pharmacology, University of Heidelberg, Federal Republic of Germany.
J Hypertens. 1989 Sep;7(9):721-6.
The mechanisms resulting in the greater predisposition of male subjects towards hypertension were investigated in different strains of rats with genetic hypertension [spontaneously hypertensive rats of the stroke-prone strain (SHRSP) and spontaneously hypertensive rats (SHR)] and their respective normotensive controls. Blood pressure was reduced in young (9 weeks of age) hypertensive rats by (1) surgical castration, (2) treatment with the testosterone receptor antagonist cyproterone acetate (CPA), which does not elevate testosterone, or (3) with the testosterone receptor antagonist flutamide, which leads to a feedback elevation of gonadotrophic hormones and plasma testosterone. These treatments had no effect on high blood pressure in old hypertensive rats aged 25 weeks. Both androgen receptor antagonists attenuated high blood pressure development when given for the first 10 days after birth. These data clearly relate the sexual dimorphism of hypertension to testosterone produced during male brain maturation in the early phase of hypertension development. Testosterone appears not to contribute directly to the maintenance of high blood pressure in established hypertension.
在患有遗传性高血压的不同品系大鼠[易中风自发性高血压大鼠(SHRSP)和自发性高血压大鼠(SHR)]及其各自的正常血压对照中,研究了导致雄性受试者更易患高血压的机制。通过以下方式降低年轻(9周龄)高血压大鼠的血压:(1)手术去势;(2)用不升高睾酮的睾酮受体拮抗剂醋酸环丙孕酮(CPA)治疗;或(3)用导致促性腺激素和血浆睾酮反馈升高的睾酮受体拮抗剂氟他胺治疗。这些治疗对25周龄的老年高血压大鼠的高血压没有影响。两种雄激素受体拮抗剂在出生后的前10天给药时,均可减弱高血压的发展。这些数据清楚地将高血压的性别差异与高血压发展早期男性大脑成熟过程中产生的睾酮联系起来。在已确诊的高血压中,睾酮似乎对维持高血压没有直接作用。