Andreis P G, Rebuffat P, Neri G, Rossi G P, Nussdorfer G G
Department of Human Anatomy and Physiology, University of Padova, Italy.
Life Sci. 2000 Jun 23;67(5):543-7. doi: 10.1016/s0024-3205(00)00648-2.
The role of angiotensin-II (Ang-II) and endothelin-1 (ET-1) in the development of hypertension and zona glomerulosa (ZG) hyperfunction in the transgenic rat strain TGR[mREN2]27 (TGR) has been investigated. Male heterozygous TGR were given per os for 4 weeks the Ang-II ATI receptor antagonist irbesartan (50 mg/kg x day) or the mixed ETA/ETB receptor antagonist bosentan (100 mg/kg x day). A group of TGR received a placebo gavage. Irbesartan lowered blood pressure (BP), while bosentan was ineffective. Conversely, both antagonists decreased plasma aldosterone concentration, the volume of ZG and its parenchymal cells, and in vitro aldosterone secretion by capsule-ZG preparations. Collectively, our results allow us to conclude that (i) only Ang-II is involved in the genesis of hypertension in TGR, while both endogenous Ang-II and ET-1 play a role in the genesis of ZG hyperfunction; and (ii) hyperaldosteronism does not contribute significantly to the development of hypertension in TGR.
血管紧张素II(Ang-II)和内皮素-1(ET-1)在转基因大鼠品系TGR[mREN2]27(TGR)高血压和肾小球带(ZG)功能亢进发展中的作用已被研究。雄性杂合TGR经口给予血管紧张素II 1型受体拮抗剂厄贝沙坦(50毫克/千克/天)或ETA/ETB混合型受体拮抗剂波生坦(100毫克/千克/天),持续4周。一组TGR接受安慰剂灌胃。厄贝沙坦可降低血压(BP),而波生坦无效。相反,两种拮抗剂均可降低血浆醛固酮浓度、ZG及其实质细胞的体积以及ZG包膜制剂的体外醛固酮分泌。总体而言,我们的结果使我们能够得出以下结论:(i)只有Ang-II参与TGR高血压的发生,而内源性Ang-II和ET-1均在ZG功能亢进的发生中起作用;(ii)高醛固酮血症对TGR高血压的发展没有显著影响。