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
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.