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PARTICIPATION OF THE RENIN‐ANGIOTENSIN SYSTEM IN REGULATING THE EXCRETORY RESPONSE TO ACUTE SODIUM INGESTION
Author(s) -
Duggan K. A.,
Jones D. M.,
MacDonald G. J.
Publication year - 1995
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.1440-1681.1995.tb02042.x
Subject(s) - medicine , sodium , endocrinology , renin–angiotensin system , angiotensin ii , chemistry , plasma renin activity , low sodium diet , low sodium , ingestion , blood pressure , organic chemistry
SUMMARY 1. A gastric sodium monitor has been proposed, based upon greater urinary sodium excretion after gastric, compared with intravenous, sodium loading. However, this difference has only been demonstrated in animals and humans on a low sodium diet prior to study. This suggests involvement of a system activated by decreased sodium intake. As the renin‐angiotensin system is the most active of these, this study sought to determine whether angiotensin II (AII) might act as a humoral mediator for this gastric sodium monitor. 2. Male New Zealand white rabbits with a gastrostomy tube in situ were placed on a low sodium diet (0.008% NaCl) for 7 days. To determine if differences in plasma AII might explain the different natriuretic responses AII was measured 0, 5,10, 30, 60 and 120 min after a 1.5mmol/kg sodium load given gastrically or intravenously. To determine whether the AII response was specific to low salt diets the gastric salt load was given after equilibration on normal (2.2% NaCl) and high (4.4% NaCl) sodium diets. 3. In rabbits on the low sodium diet plasma AII decreased significantly at 5 min after both gastric ( P < 0.025) and intravenous ( P < 0.05) sodium and returned to baseline by 10 min in the latter. In contrast after gastric sodium AII remained less than in controls throughout (120 min, P < 0.05). In the rabbits on the normal and high sodium diets plasma AII concentration increased non‐significantly after gastric sodium administration. 4. We conclude that circulating AII may participate as a mediator of the gastric sodium monitor. Its concentration was reduced and remained persistently lower after gastric but not intravenous sodium. Further, this change was not apparent on sodium diets in which differences in sodium excretion have not been demonstrated previously.