Renin-aldosterone axis and arginine-vasopressin responses to sodium depletion in camels

Urinary output, urinary sodium and potassium excretion, plasma electrolyte concentrations and osmolality, plasma renin activity (PRA), and plasma aldosterone and arginine-vasopressin (AVP) concentrations were determined in eight camels in Tadla (Morocco). After administration of furosemide (2 mg.kg-...

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Bibliographic Details
Published in:General and comparative endocrinology Vol. 95; no. 2; p. 240
Main Authors: Riad, F, Ben Goumi, M, Giry, J, Davicco, M J, Safwate, A, Barlet, J P
Format: Journal Article
Language:English
Published: United States 01-08-1994
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Summary:Urinary output, urinary sodium and potassium excretion, plasma electrolyte concentrations and osmolality, plasma renin activity (PRA), and plasma aldosterone and arginine-vasopressin (AVP) concentrations were determined in eight camels in Tadla (Morocco). After administration of furosemide (2 mg.kg-1 body wt) urinary water, sodium and potassium excretions increased, inducing hypovolemia (as reflected by 14.6% increase in hematocrit), hyponatremia (142 +/- 1.0 vs 150 +/- 2.1 mmol.liter-1 in controls; P < 0.05), plasma hypo-osmolality (287.5 +/- 11.5 vs 307 +/- 1.4 mOsm.kg-1 H2O in controls; P < 0.05), and hypokalemia (3.7 +/- 0.2 vs 4.6 +/- 0.1 mmol.liter-1 in controls; P < 0.05). Such body fluid volume and composition changes were associated with parallel increases in PRA and plasma aldosterone concentrations (5.9 +/- 0.6 vs 0.9 +/- 0.2 ng AI.ml-1.hr-1 and 132.4 +/- 35.5 vs 25.1 +/- 6.5 pg.ml-1 in controls, respectively; P < 0.05). They were also associated with a fourfold increase in plasma arginine-vasopressin concentrations (0.8 +/- 0.2 vs 0.2 +/- 0.1 pg.ml-1; P < 0.05). In furosemide-treated animals, plasma aldosterone concentrations correlated positively with PRA (r = 0.85; n = 64; P < 0.01) and negatively with plasma sodium concentrations (r = -0.80; n = 64; P < 0.01), suggesting that in sodium-depleted camels the nexus between the renin-angiotensin system and aldosterone was restored.
ISSN:0016-6480
DOI:10.1006/gcen.1994.1121