Adrenergic regulation of renin secretion and renal hemodynamics during deliberate hypotension in humans.
Adrenergic regulation of renin secretion and renal hemodynamics during deliberate hypotension in humans.
复制标题
人故意低血压期间肾素分泌和肾血流动力学的肾上腺素调节。
DOI：
10.1152/ajprenal.1993.265.5.f686
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Laragh,JH
中科院分区：
文献类型：
--
作者：
Zayas,VM;Blumenfeld,JD;Bading,B;McDonald,M;James,GD;Lin,YF;Sharrock,NE;Sealey,JE;Laragh,JH
To assess the relative contributions of neural and nonneural stimuli of renin secretion, the effects of an alpha 1-agonist, phenylephrine (Phe), or a beta-agonist, epinephrine (Epi), on plasma renin activity (PRA), renal blood flow (RBF), and glomerular filtration rate (GFR) were compared during sympathetic blockade with epidural hypotensive anesthesia [mean arterial blood pressure (MAP) = 60 and 50 mmHg]. Controls (NaCl) received saline alone to maintain MAP at 50 mmHg. Epi increased PRA (ng.ml-1.h-1) from 0.9 +/- 0.6 to 3.0 +/- 1.5 at 60 mmHg MAP and 4.7 +/- 1.8 at 50 mmHg MAP, with associated decreases in RBF (-33 and -60%, respectively) and GFR (-27 and -53%, respectively). During hypotension with Phe and NaCl, PRA and RBF were unchanged from baseline but GFR decreased. Urinary Na secretion decreased comparably in all three groups. In conclusion, during sympathetic blockade with epidural anesthesia, marked reductions in both renal perfusion pressure and distal nephron Na delivery were insufficient to increase renin secretion. beta-Adrenergic stimulation (e.g., Epi) was required to increase PRA. Epi decreased RBF suggesting an angiotensin II-mediated effect.
