AJP - Regulatory, Integrative and Comparative Physiology, Vol 264, Issue 3 492-R499, Copyright © 1993 by American Physiological Society
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.
