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Am J Physiol Regul Integr Comp Physiol 264: R492-R499, 1993;
0363-6119/93 $5.00
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AJP - Regulatory, Integrative and Comparative Physiology, Vol 264, Issue 3 492-R499, Copyright © 1993 by American Physiological Society

ARTICLES

Independence of salt intake induced by calcium deprivation from the renin-angiotensin-aldosterone system

M. G. Tordoff, D. M. Pilchak and R. L. Hughes
Monell Chemical Senses Center, Philadelphia, Pennsylvania 19104-3308.

We investigated whether the elevated NaCl intake shown by calcium-deprived rats is mediated by the renin-angiotensin-aldosterone system. First, we looked for manifestations of altered renin-angiotensin-aldosterone system activity during the progression of calcium deficiency. There were no differences between control and calcium-deprived rats in plasma aldosterone concentrations, plasma renin activity, plasma sodium concentrations, sodium balance, or blood pressure. Second, we used selective pharmacological antagonists to examine whether disruption of the renin-aldosterone-angiotensin system influenced salt intake. Blockade of aldosterone receptors with spironolactone (25 mg.kg-1 x day-1 sc for 7 days) had no effect on NaCl intake of control or calcium-deprived rats. Angiotensin AT1 receptor blockade with losartan potassium (0.5-10 mg/kg orally) had no effect on NaCl intake of control or calcium-deprived rats but doses > 0.5 mg/kg decreased NaCl intake of adrenalectomized rats. Taken together, these findings indicate that the renin-angiotensin-aldosterone system does not mediate the increased NaCl intake produced by calcium deficiency. The appetite for salt produced by calcium deficiency involves a different physiological substrate from most other models of NaCl intake.


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