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1 Basic Biomedical Sciences, University of South Dakota, Vermillion, SD 57069, USA
* To whom correspondence should be addressed. E-mail: dsmartin{at}usd.edu.
Males develop higher blood pressure than do females. This study tested the hypothesis that androgens enhance responsiveness to angiotensin II (Ang II) during the development of hypertension in New Zealand genetically hypertensive rats (NZGH). Male NZGH were obtained at 5 weeks of age and subjected to sham operation (Sham) or castration (Cas) then studied at three age groups: 6-7, 11-12 and 16-17 weeks. Arterial pressure (MAP), heart rate (HR) and renal blood flow (RBF) measurements were recorded under Inactin anesthesia. These variables were measured following enalapril (1mg/kg) treatment and during intravenous angiotensin II (Ang II) infusion (20, 40 and 80 ng/kg/min). Plasma testosterone was measured by ELISA. Angiotensin AT1 receptor expression was assessed by Western blot and RT-PCR. Ang II-induced MAP responses were significantly attenuated in Cas NZGH. At the highest Ang II dose, MAP increased by 40±4% in Sham versus 22±1% in Cas NZGH of 16-17 weeks of age. Similarly, renal vascular resistance (RVR) responses to Ang II were reduced by castration (209±20% in Sham versus 168±10% in Cas NZGH at 16-17 weeks of age). Castration also reduced MAP recorded in conscious NZGH of this age group. Testosterone replacement restored baseline MAP and the pressor and RVR responses to Ang II. Castration reduced testosterone concentrations markedly. Testosterone treatment restored these concentrations. Neither castration or castration+testosterone treatment affected AT1 receptor mRNA or protein expression. Collectively, these data suggest that androgens modulate renal and systemic vascular responsiveness to Ang II which may contribute to androgen-induced facilitation of NZGH hypertension.
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