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MECHANISMS UNDERLYING THE DECREASE IN CIRCULATING ANGIOTENSIN II CONCENTRATION AFTER SODIUM LOADING
Author(s) -
Duggan KA,
Ye VZC
Publication year - 1998
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1998.tb02159.x
Subject(s) - endocrinology , medicine , sodium , chemistry , angiotensin ii , renin–angiotensin system , catabolism , metabolism , blood pressure , organic chemistry
SUMMARY 1. Acute sodium loading causes a rapid decrease in the circulating concentration of angiotensin II (AngII), which is apparent from 5 min after sodium administration. This could result from an increase in AngII catabolism and/or a decrease in AngII synthesis/secretion. However, the major determinant of AngII synthesis is thought to be a change in plasma renin activity, which occurs over a longer time frame (15 min). 2. To investigate the mechanisms underlying the rapid decrease in plasma AngII engendered by sodium administration, we performed metabolic clearance studies in male New Zealand white rabbits before and after a hypertonic sodium load of 1.5 mmol/kg as 0.513 mol/L saline i.v. bolus. 3. The metabolic clearance rate of AngII increased significantly from 42.2 ± 9.0 mL/min per kg before sodium to 110.8±33.7 mL/min per kg after sodium administration ( P <0.05). The calculated or theoretical secretion rate decreased from 1470.7±404.2 to 573.5 ± 139.5 fmol/min per kg ( P <0.025) in response to sodium. 4. We conclude that an increase in AngII metabolism and a decrease in synthesis/secretion contribute to the reduction in circulating AngII, which occurs in the first 60–90 min after sodium loading.