Physiology & Behavior, Vol. 49, pp. 113-115. ©PergamonPressplc, 1991.Printedin the U.S.A.
0031-9384/91 $3.00 + .00
Calcium Deprivation Increases NaC1 Intake of Fischer-344 Rats MICHAEL G. TORDOFF Monell Chemical Senses Center, 3500 Market St., Philadelphia, PA 19104-3308 Received 16 July 1990
TORDOFF, M. G. Calcium deprivation increases NaCl intake of Fischer-344 rats. PHYSIOL BEHAV 49(1) 113-115, 1991.Fischer-344 rats fed Ca2+-deficientdiet for 63 days increased intake of 0.3 M NaC1 solution from control levels of - 8 ml/day to >60 ml/day. During the same period, rats fed Na+-deficient diet drank ~11 ml/day. These results indicate that Fischer-344 rats, which generallyspurn NaCI, drink large amountsof it when Ca2+ deprived. Salt intake
Sodium
Strain differences
Calcium
FISCHER-344 rats differ from other strains used to study ingestive behavior in that they show little spontaneous intake of dilute NaC1 solution (6--8). Despite this, they respond to manipulations of the renin-angiotensin-aldosterone system such as adrenalectomy, dietary Na + restriction, or treatment with furosemide, deoxycorticosterone acetate, or angiotensin converting enzyme inhibitors [(7,8); reviews (9,10)]. Their response to these manipulations tends to be blunted relative to those of other strains, but it is still sufficient to satisfy Na + homeostasis. Recently, we found that a potent control of NaC1 intake is provided by some aspect of Ca2 + metabolism. Sprague DawIcy rats fed low-Ca2+ diets dramatically increase their voluntary NaC1 intake. These animals have normal plasma concentrations of Na +, aldosterone, and angiotensin I, and they retain Na + more efficiently than do controls (12). Given that neither the low NaC1 intake of Fischer-344 rats nor the high NaC1 intake of Ca2÷-deficient Sprague Dawley rats can easily be accounted for by dysfunctions of the renin-angiotensin-aldosteronesystem, it seemed worthwhile examining if Fischer-344 rats were sensitive to the effects of Ca2+ deprivation. METHOD The subjects were 28 male Fischer-344 rats, purchased from Charles River (Kingston, NY), weighing 67-88 g at the start of the experiment. They were housed individually in stainless steel cages and maintained at ~21°C on a 12:12-h light/dark cycle (lights off at 7:00 p.m.). Food was provided as a powder in glass jars held in the rats' cages by steel springs. Water and 0.3 M NaC1 were provided in glass bottles with stainless steel drinking spouts. The rats initially ate Purina Laboratory Chow (No. 5001) and drank tap water for 6 days so that they could adapt to laboratory conditions. They then received unlimited access to both deionized water and 0.3 M NaCI for another 6 days. After this baseline period, they continued to have access to deionized water and 0.3 M NaCI, but for 63 days, their chow was replaced with Ca2+-deficient (n=9), Na+-deficient (n=9) or AIN-76A control (n= 10) diet.
The deficient diets were modified versions of the AIN-76A formulation (1), prepared by Dyets Inc. (Bethlehem, PA) with mineral-free casein. AIN-76A diet contains per kilogram ~ 130 mmol Ca2+, 44 mmol Na +, and 92 mmol K +. The Na +-deficient diet was prepared by omission of NaC1 from the mineral mix, leaving
0031-9384/91 $3.00 + .00
Calcium Deprivation Increases NaC1 Intake of Fischer-344 Rats MICHAEL G. TORDOFF Monell Chemical Senses Center, 3500 Market St., Philadelphia, PA 19104-3308 Received 16 July 1990
TORDOFF, M. G. Calcium deprivation increases NaCl intake of Fischer-344 rats. PHYSIOL BEHAV 49(1) 113-115, 1991.Fischer-344 rats fed Ca2+-deficientdiet for 63 days increased intake of 0.3 M NaC1 solution from control levels of - 8 ml/day to >60 ml/day. During the same period, rats fed Na+-deficient diet drank ~11 ml/day. These results indicate that Fischer-344 rats, which generallyspurn NaCI, drink large amountsof it when Ca2+ deprived. Salt intake
Sodium
Strain differences
Calcium
FISCHER-344 rats differ from other strains used to study ingestive behavior in that they show little spontaneous intake of dilute NaC1 solution (6--8). Despite this, they respond to manipulations of the renin-angiotensin-aldosterone system such as adrenalectomy, dietary Na + restriction, or treatment with furosemide, deoxycorticosterone acetate, or angiotensin converting enzyme inhibitors [(7,8); reviews (9,10)]. Their response to these manipulations tends to be blunted relative to those of other strains, but it is still sufficient to satisfy Na + homeostasis. Recently, we found that a potent control of NaC1 intake is provided by some aspect of Ca2 + metabolism. Sprague DawIcy rats fed low-Ca2+ diets dramatically increase their voluntary NaC1 intake. These animals have normal plasma concentrations of Na +, aldosterone, and angiotensin I, and they retain Na + more efficiently than do controls (12). Given that neither the low NaC1 intake of Fischer-344 rats nor the high NaC1 intake of Ca2÷-deficient Sprague Dawley rats can easily be accounted for by dysfunctions of the renin-angiotensin-aldosteronesystem, it seemed worthwhile examining if Fischer-344 rats were sensitive to the effects of Ca2+ deprivation. METHOD The subjects were 28 male Fischer-344 rats, purchased from Charles River (Kingston, NY), weighing 67-88 g at the start of the experiment. They were housed individually in stainless steel cages and maintained at ~21°C on a 12:12-h light/dark cycle (lights off at 7:00 p.m.). Food was provided as a powder in glass jars held in the rats' cages by steel springs. Water and 0.3 M NaC1 were provided in glass bottles with stainless steel drinking spouts. The rats initially ate Purina Laboratory Chow (No. 5001) and drank tap water for 6 days so that they could adapt to laboratory conditions. They then received unlimited access to both deionized water and 0.3 M NaCI for another 6 days. After this baseline period, they continued to have access to deionized water and 0.3 M NaCI, but for 63 days, their chow was replaced with Ca2+-deficient (n=9), Na+-deficient (n=9) or AIN-76A control (n= 10) diet.
The deficient diets were modified versions of the AIN-76A formulation (1), prepared by Dyets Inc. (Bethlehem, PA) with mineral-free casein. AIN-76A diet contains per kilogram ~ 130 mmol Ca2+, 44 mmol Na +, and 92 mmol K +. The Na +-deficient diet was prepared by omission of NaC1 from the mineral mix, leaving
