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AJP - Regulatory, Integrative and Comparative Physiology, Vol 269, Issue 6 1351-R1355, Copyright © 1995 by American Physiological Society
ARTICLES |
B. A. Benjamin and T. V. Peterson
Department of Cell Biology, Duke University Medical Center, Durham, North Carolina 27710, USA.
The purpose of this study was to determine the effect of proANF-(31--67) on renal function in conscious, chronically instrumented monkeys (Macaca fascicularis). The experimental protocol consisted of a 30-min control period followed by 60 min of peptide infusion and a 30-min recovery period. Atrial natriuretic factor (ANF)-(99--126), proANF-(31--67), of a combination of ANF-(99--126) plus proANF-(31--67) was infused at 15 pmol.kg-1.min-1. ANF-(99--126) caused sodium excretion to increase from 12.5 +/- 3 to a peak of 37.9 +/- 10.4 mueq/min, whereas fractional sodium excretion (FENa) increased from 0.69 +/- 0.2 to 2.3 +/- 0.43%. ProANF-(31--67) increased sodium excretion from 12.7 +/- 5 to a peak of 23.3 +/- 9.0 mueq/min and FENa from 0.56 +/- 0.07 to a peak of 1.15 +/- 0.4%. When ANF-(99--126) and proANF-(31--67) were infused in combination, sodium excretion increased from 9.6 +/- 3 to a peak of 5.19 +/- 12.5 mueq/min, whereas FENa increased from 0.97 +/- 0.4 to 3.9 +/- 1.1%. Mean arterial pressure decreased by approximately 10 mmHg in all three groups. These findings indicate that intravenously administered proANF-(31--67) causes an increase in sodium excretion and that when proANF-(31--67) and ANF-(99--126) are given in combination, they act in an additive fashion to increase renal sodium excretion.
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