Tallam L S, Jandhyala B S
Institute for Cardiovascular Studies, University of Houston, TX 77204-5515, USA.
Clin Exp Hypertens. 2001 Nov;23(8):623-31. doi: 10.1081/ceh-100107392.
Salt-sensitive individuals are susceptible to develop hypertension when exposed to high salt-diet. Such a phenomenon is considered to be due to a genetic impairment in the renal excretion of sodium. In the present studies extent of endogenous angiotensin-II (Ang-II) mediated antinatriuresis was comparatively evaluated in Dahl salt-sensitive (SS) and salt-resistant (SR) rats, using a selective AT1 receptor antagonist, candesartan. In addition, differences in plasma renin activity and characteristics of Ang-II receptors in the renal cortical tubular membranes were also examined. Under INACTIN anesthesia AT1 receptor blockade resulted in significant increases in renal sodium excretion, which was several-fold greater in SS rats than that observed in SR rats. These observations suggest that antinatriuretic function of endogenous angiotensin-II is exaggerated in SS rats. This functional overexpression appears to be related to an increase in the affinity of Ang-II receptors in renal cortical tubular membranes but not to receptor density or plasma renin activity. It is proposed that salt-dependent hypertension in Dahl salt-sensitive rats may be due to enhanced Ang-II mediated sodium retention.
盐敏感个体在摄入高盐饮食时易患高血压。这种现象被认为是由于肾脏排钠的基因缺陷所致。在本研究中，使用选择性AT1受体拮抗剂坎地沙坦，比较评估了 Dahl 盐敏感（SS）大鼠和盐抵抗（SR）大鼠内源性血管紧张素 II（Ang-II）介导的利钠作用程度。此外，还检测了血浆肾素活性以及肾皮质肾小管膜中 Ang-II 受体特性的差异。在 INACTIN 麻醉下，AT1 受体阻断导致肾钠排泄显著增加，SS 大鼠的增加幅度是 SR 大鼠的几倍。这些观察结果表明，内源性血管紧张素 II 的利钠作用在 SS 大鼠中被夸大。这种功能的过度表达似乎与肾皮质肾小管膜中 Ang-II 受体亲和力的增加有关，而与受体密度或血浆肾素活性无关。有人提出，Dahl 盐敏感大鼠的盐依赖性高血压可能是由于 Ang-II 介导的钠潴留增强所致。
