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AJP - Renal Physiology, Vol 251, Issue 3 532-F536, Copyright © 1986 by American Physiological Society
ARTICLES |
F. J. Salazar, M. J. Fiksen-Olsen, T. J. Opgenorth, J. P. Granger, J. C. Burnett Jr and J. C. Romero
The aim of the present study was to determine if atrial natriuretic peptide (ANP)-induced natriuresis is dependent on increases in glomerular filtration rate (GFR). Intrarenal blood flow distribution and urinary excretion of prostaglandins were also determined during the infusion of a dose of ANP that does not induce changes in GFR and mean arterial pressure (MAP). It was found that the intrarenal infusion of ANP (8-33) at a dose of 0.05 micrograms X kg-1. min-1 in seven anesthetized dogs did not produce any change in GFR or MAP, but its natriuretic effect was similar to that obtained by a larger dose (0.3 micrograms X kg-1 X min-1, n = 5) that produces significant changes in both MAP and GFR. The natriuresis induced by the lower dose of ANP was associated with a redistribution (P less than 0.05) of renal blood flow (RBF) from the superficial to the juxtamedullary cortex and with an increase (P less than 0.05) in urinary excretion of prostaglandins E2 (PGE2) (0.8 +/- 0.2 to 2.4 +/- 1.0 ng/min) and 6-keto-F1 alpha (6-keto-PGF1 alpha) (2.8 +/- 0.6 to 5.5 +/- 1.7 ng/min). Renin secretion rate decreased from 610 +/- 165 to 279 +/- 61 ng angiotensin I/min. These results show that the natriuresis induced by ANP is not necessarily produced by an increase in GFR and is associated with a redistribution of RBF to the deep cortex and an increase in urinary excretion of PGE2 and 6-keto-PGF1 alpha.
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