Effect of Renal Nerve Stimulation on Renal Blood Flow Autoregulation and Antinatriuresis During Reductions in Renal Perfusion Pressure (41238)

Jeffrey L. Osborn, Linda L. Francisco, Gerald F. Dibona

Research output: Contribution to journalArticlepeer-review

20 Scopus citations

Abstract

Renal nerve stimulation increases renal vascular resistance and decreases glomerular filtration rate and urinary sodium excretion. The purpose of this study was to determine whether neurally mediated changes in renal vascular resistance, glomerular filtration rate, and urinary sodium excretion at control renal perfusion pressure modified the autoregulation of renal blood flow and glomerular filtration rate and the antinatriuresis observed during reductions in renal perfusion pressure in pentobarbital-anesthetized dogs. Renal blood flow, glomerular filtration rate, and urinary sodium excretion were determined during stepwise reductions in renal perfusion pressure from 137 to 55 mm Hg (suprarenal aortic constriction) before and during electrical stimulation of the renal nerves at 0.5, 1.0, 2.0, and 4.0 Hz. In the absence of renal nerve stimulation, renal blood flow and glomerular filtration rate remained constant until renal perfusion pressure was reduced to 70 and 85 mm Hg, respectively. Urinary sodium excretion decreased linearly as renal perfusion pressure decreased. Renal nerve stimulation at 0.5, 1.0, 2.0, and 4.0 Hz increased renal vascular resistance and decreased glomerular filtration rate and urinary sodium excretion. These frequencies of renal nerve stimulation, however, did not alter the decreases in renal vascular resistance and glomerular filtration rate or the antinatriuretic response to stepwise reductions in renal perfusion pressure to 55 mm Hg. These data demonstrate that increased renal vascular resistance at either the afferent or efferent arteriole does not change the responses of these vessels to reductions in renal perfusion pressure. Renal nerve stimulation at frequencies which decrease urinary sodium excretion at control renal perfusion pressure also does not enhance the antinatriuretic response to reductions in renal perfusion pressure.

Original languageEnglish
Pages (from-to)77-81
Number of pages5
JournalProceedings of the Society for Experimental Biology and Medicine
Volume168
Issue number1
DOIs
StatePublished - Oct 1981

ASJC Scopus subject areas

  • General Biochemistry, Genetics and Molecular Biology

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