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AJP - Regulatory, Integrative and Comparative Physiology, Vol 270, Issue 3 505-R517, Copyright © 1996 by American Physiological Society
ARTICLES |
M. G. Tordoff and A. Okiyama
Monell Chemical Senses Center, Philadelphia, Pennsylvania 19104, USA.
To assess daily rhythms of salt appetite, we measured spontaneous 300 mM NaCl intake of male Sprague-Dawley rats fed a diet containing 150 or 25 mmol Ca2+/kg. Both groups drank most NaCl at night, but, as the dark period progressed, intakes of controls remained constant or diminished, whereas intakes of rats fed low-Ca2+ diet increased. During the late dark period, when the difference in NaCl intake between the two dietary groups was greatest, rats fed a low-Ca2+ diet lost more corticosterone and sodium in urine, had lower plasma osmolarity, and had higher plasma adrenocorticotropic hormone (ACTH) and corticosterone concentrations than did controls. Over the 24-h cycle, rats fed the low-Ca2+ diet excreted less Ca2+ and more corticosterone in urine than did controls. They also had consistently lower plasma concentrations of Ca2+ and renin activity and consistently higher plasma phosphorus, arginine vasopressin, parathyroid hormone, thyroxine, calcitonin, and 1,25-dihydroxyvitamin D3. These findings support the hypothesis that salt appetite induced by dietary Ca2+ deficiency involves a subtle dysfunction of the ACTH-corticosterone axis, but they also raise several other possibilities.
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