PARTICIPATION OF THE RENIN-ANGIOTENSIN SYSTEM IN REGULATING THE EXCRETORY RESPONSE TO ACUTE SODIUM INGESTION

Citation
Ka. Duggan et al., PARTICIPATION OF THE RENIN-ANGIOTENSIN SYSTEM IN REGULATING THE EXCRETORY RESPONSE TO ACUTE SODIUM INGESTION, Clinical and experimental pharmacology and physiology, 22(6-7), 1995, pp. 455-456
Citations number
6
Categorie Soggetti
Pharmacology & Pharmacy",Physiology
ISSN journal
03051870
Volume
22
Issue
6-7
Year of publication
1995
Pages
455 - 456
Database
ISI
SICI code
0305-1870(1995)22:6-7<455:POTRSI>2.0.ZU;2-X
Abstract
1. A gastric sodium monitor has been proposed, based upon greater urin ary sodium excretion after gastric, compared with intravenous, sodium loading. However, this difference has only been demonstrated in animal s and humans on a low sodium diet prior to study, This suggests involv ement of a system activated by decreased sodium intake. As the renin-a ngiotensin system is the most active of these, this study sought to de termine whether angiotensin II (AII) might act as a humoral mediator f or 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% N aCl) for 7 days, To determine if differences in plasma AII might expla in the different natriuretic responses AII was measured 0, 5, 10, 30, 60 and 120 min after a 1.5 mmol/kg sodium load given gastrically or in travenously. To determine whether the AII response was specific to low salt diets the gastric salt load was given after equilibration on nor mal (2.2% NaCl) and high (4.4% NaCl) sodium diets. 3. In rabbits on th e low sodium diet plasma AII decreased significantly at 5 min after bo th gastric (P<0.025) and intravenous (P<0.05) sodium and returned to b aseline 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 ra bbits on the normal and high sodium diets plasma AII concentration inc reased non-significantly after gastric sodium administration. 4. We co nclude that circulating AII may participate as a mediator of the gastr ic sodium monitor. Its concentration was reduced and remained persiste ntly lower after gastric but not intravenous sodium, Further, this cha nge was not apparent on sodium diets in which differences in sodium ex cretion have not been demonstrated previously.