Adrenergic regulation of renin secretion and renal hemodynamics during deliberate hypotension in humans. Academic Article uri icon

Overview

abstract

  • 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.

publication date

  • November 1, 1993

Research

keywords

  • Epinephrine
  • Hemodynamics
  • Hypotension
  • Kidney
  • Phenylephrine
  • Renal Circulation
  • Renin

Identity

Scopus Document Identifier

  • 0027423945

Digital Object Identifier (DOI)

  • 10.1152/ajprenal.1993.265.5.F686

PubMed ID

  • 8238548

Additional Document Info

volume

  • 265

issue

  • 5 Pt 2