Influence of angiotensin II on pressure natriuresis and renal hemodynamics in volume-expanded rats

D. L. Mattson, H. Raff, R. J. Roman

Research output: Contribution to journalArticle

53 Scopus citations

Abstract

This study examined whether angiotensin II (ANG II) influences the pressure-natriuretic (PN) response by altering renal cortical or medullary hemodynamics. Studies were performed in Inactin-anesthetized rats that were acutely volume expanded to maintain plasma renin activity and ANG II levels in the physiological range. Neural influences on the kidney were eliminated by renal denervation, and plasma levels of norepinephrine, vasopressin, cortisol, and aldosterone were fixed by intravenous infusion. In control rats (n = 8), sodium excretion increased from 3 to 17 μeq·min-1·g kidney wt-1 as renal perfusion pressure (RPP) was elevated from 96 to 141 mmHg (n = 8). Captopril (2 mg/kg, n = 9) reduced plasma levels of ANG II from 48 ± 5 to 18 ± 2 pg/ml, but it did not alter the PN relationship. Infusion of ANG II (20 ng·kg-1·min-1, n = 9) increased plasma levels of ANG II to 232 ± 42 pg/ml and shifted the PN relationship to the right by 14 mmHg. Captopril increased renal blood flow, and infusion of ANG II returned it to control. Captopril had no effect on glomerular filtration rate (GFR) or glomerular capillary pressure (P(glom)); however, subsequent ANG II infusion decreased P(glom) from 56 ± 2 to 48 ± 2 mmHg and reduced GFR by 30%. Neither captopril nor ANG II altered papillary bloodflow or vasa recta capillary pressure at normal levels of RPP. These results indicate that the shift of the PN relationship during infusion of ANG II is due to a decrease in filtered load and enhanced tubular reabsorption of sodium. Acute blockade of the renin-angiotensin system had little effect on the PN response in volume-expanded rats despite affecting renal hemodynamics, because either the plasma and/or intrarenal levels of ANG II were already suppressed below those needed to influence tubular function or volume expansion inhibits tubular reabsorption in the nephron segments normally influenced by ANG II.

Original languageEnglish (US)
Pages (from-to)R1200-R1209
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume260
Issue number6 29-6
DOIs
StatePublished - 1991
Externally publishedYes

Keywords

  • Captopril
  • Kidney
  • Renal hypertension
  • Renal medulla

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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