ETA receptor-mediated role of endothelin in the kidney of DOCA-salt hypertensive rats.
ETA receptor-mediated role of endothelin in the kidney of DOCA-salt hypertensive rats.
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DOCA-盐高血压大鼠肾脏中 ETA 受体介导的内皮素作用。
DOI：
10.1016/0024-3205(95)02259-7
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发表时间：
1995
期刊：
影响因子：
6.1
通讯作者：
Shiro Morimoto
中科院分区：
文献类型：
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作者：
K. Fujita;Yasuo Matsumura;Yohko Miyazaki;N. Hashimoto;M. Takaoka;Shiro Morimoto
采用麻醉的正常血压大鼠和醋酸脱氧皮质酮（DOCA）盐性高血压大鼠，观察内皮素ETA受体拮抗剂FR 139317对肾脏的影响。静脉推注FR 139317（10 mg/kg）导致对照大鼠的平均血压（MAP; −13%）轻微降低，这种低血压伴有中度肾血管舒张（肾血管阻力：RVR; −12%）。在DOCA盐高血压大鼠中，FR 139317具有更明显的舒张作用（MAP; −26%），并伴有强效肾血管舒张（RVR; −33%）。FR 139317仅在DOCA盐大鼠中显著增加肾血流量。相比之下，FR 139317仅在对照大鼠中产生尿流量和尿钠排泄的显著降低。北方印迹分析显示DOCA盐性高血压大鼠肾组织ET-1 mRNA表达显著增加。因此，内源性ET-1可能是DOCA盐诱导的高血压维持的原因。我们还认为，至少部分地，ET-1和Eta受体参与DOCA盐诱导的高血压的肾血流动力学异常。肾脏ET-1生成的增加可能在DOCA盐诱导的高血压的发展和维持中起作用。
Renal effects of FR139317, an endothelin ETAreceptor antagonist, were examined using anesthetized normotensive and deoxycorticosterone acetate (DOCA)-salt hypertensive rats. The intravenous bolus injection of FR139317 (10 mg/kg) produced a slight decrease in mean blood pressure (MAP; −13%) in the control rats and this hypotension was accompanied by a moderate renal vasodilation (renal vascular resistance: RVR; −12%). In the DOCA-salt hypertensive rat, FR139317 had a more pronounced hypotensive effect (MAP; −26%) accompanied by a potent renal vasodilation (RVR; −33%). FR 139317 significantly increased renal blood flow only in the DOCAsalt rats. In contrast, FR139317 produced a significant decrease in urine flow and urinary sodium excretion only in control rats. Northern blot analysis revealed that the renal prepro endothelin-1 (ET-1) mRNA level was significantly increased in DOCA-salt hypertensive rats. Thus, it seems likely that endogenous ET-1 is responsible for the maintenance of DOCA-salt-induced hypertension. We also suggest that at least in part, ET-1 and £ta receptors are involved in renal hemodynamic abnormalities in DOCA-salt-induced hypertension. The augmentation of renal ET-1 production may possibly have a function in the development and maintenance of DOCA-salt-induced hypertension.
DOI：
10.1681/asn.v22150
发表时间：
1991
期刊：
Journal of the American Society of Nephrology : JASN
影响因子：
--
作者：
Kohan,DE;FiedorekJr,FT
通讯作者：
FiedorekJr,FT