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首页> 外文期刊>American Journal of Physiology >Androgens augment renal vascular responses to ANG II in New Zealand genetically hypertensive rats.
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Androgens augment renal vascular responses to ANG II in New Zealand genetically hypertensive rats.

机译：雄激素增强了新西兰遗传性高血压大鼠对ANG II的肾脏血管反应。

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摘要

Males develop higher blood pressure than do females. This study tested the hypothesis that androgens enhance responsiveness to ANG II during the development of hypertension in New Zealand genetically hypertensive (NZGH) rats. Male NZGH rats were obtained at 5 wk of age and subjected to sham operation (Sham) or castration (Cas) then studied at three age groups: 6-7, 11-12, and 16-17 wk. Mean arterial blood pressure (MAP), heart rate (HR), and renal blood flow (RBF) measurements were recorded under Inactin anesthesia. These variables were measured after enalapril (1 mg/kg) treatment and during intravenous ANG II infusion (20, 40, and 80 ng/kg/min). Plasma testosterone was measured by ELISA. Angiotensin type 1 (AT1) receptor expression was assessed by Western blot analysis and RT-PCR. ANG II-induced MAP responses were significantly attenuated in Cas NZGH rats. At the highest ANG II dose, MAP increased by 40+/-4% in Sham vs. 22+/-1% in Cas NZGH rats of 16-17 wk of age. Similarly, renal vascular resistance (RVR) responses to ANG II were reduced by castration (209+/-20% in Sham vs. 168+/-10% in Cas NZGH rats at 16-17 wk of age). Castration also reduced MAP recorded in conscious NZGH rats 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 nor 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 rat hypertension.
机译：男性的血压高于女性。这项研究检验了以下假设：在新西兰遗传性高血压（NZGH）大鼠中，雄激素增强了高血压形成过程中对ANG II的反应性。在5周龄时获得雄性NZGH大鼠，并进行假手术（Sham）或去势（Cas），然后在三个年龄组：6-7、11-12和16-17周进行研究。在Inactin麻醉下记录平均动脉压（MAP），心率（HR）和肾血流量（RBF）。在依那普利（1 mg / kg）治疗后和静脉ANG II输注期间（20、40和80 ng / kg / min）测量这些变量。通过ELISA测量血浆睾丸激素。通过Western印迹分析和RT-PCR评估1型血管紧张素（AT1）受体的表达。 ANG II诱导的MAP反应在Cas NZGH大鼠中显着减弱。在最高的ANG II剂量下，Sham的MAP升高40 +/- 4％，而16-17周龄的Cas NZGH大鼠的MAP升高22 +/- 1％。类似地，去势可降低对ANG II的肾血管抵抗（RVR）反应（Sham组为209 +/- 20％，Cas NZGH大鼠为16-17周龄时为168 +/- 10％）。去势还降低了该年龄组的清醒NZGH大鼠中记录的MAP。睾丸激素替代治疗可恢复基线MAP以及对ANG II的升压和RVR反应。去势明显降低了睾丸激素的浓度。睾丸激素治疗恢复了这些浓度。去势或去势+睾丸激素治疗均不影响AT1受体mRNA或蛋白表达。总体而言，这些数据表明，雄激素调节肾和全身血管对ANG II的反应，这可能有助于雄激素诱导的NZGH大鼠高血压的缓解。

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