Potassium intake during cell dehydration.

Isotonic NaCl is ingested in addition to water by cell-dehydrated rats in two-bottle tests. The objective of the present work was to find out whether mineral intake in the cell-dehydrated rat is specific to NaCl in a five-bottle test. Adult male Sprague Dawley rats had distilled water and four mineral solutions at palatable concentrations (0.01 M KCl, 0.05 mM CaCl2, 0.15 M NaHCO3, 0.15 M NaCl) simultaneously available for consumption. Cell-dehydration was produced infusing 1.5 ml of NaCl solution (0.15, 0.25, 0.5, 1.0, 2.0, 4.0 M) intravenously for 10 min and intakes were recorded for the next hour. It was observed a NaCl concentration-dependent increase in 0.01 M KCl intake. The ingestion of the other mineral solutions was not significantly altered compared to infusion of 0.15 M NaCl. The ingestion of KCl was not related to changes in serum potassium concentration. The ingestion of KCl was reduced in half and water was the preferred fluid when the five-bottle test was performed with mineral solutions at isomolar (0.15 M) concentrations. There was no increase in intake of other mineral solution in the isomolar test. No preference was observed for palatable or isomolar solutions during early extracellular dehydration until 4 h after subcutaneous injection of furosemide, in spite of the increase in total volume intake. Therefore, mineral intake induced by cell dehydration is not specific for NaCl solution. The type of mineral solution available influences the choice and KCl is the preferred solution of the cell-dehydrated rat in the conditions of the present study.

Interaction between brain L-type calcium channels and alpha2-adrenoceptors in the inhibition of sodium appetite.

Calcium channels mediate the actions of many drugs. The present work investigated whether diltiazem, an L-type calcium channel blocker, alters the inhibition of sodium appetite induced by noradrenaline and the alpha2-adrenoceptor agonist clonidine. Adult male Holtzman rats (N=4-8) with cannula implanted into the third cerebral ventricle were submitted to sodium depletion (furosemide sc+24-h removal of ambiente sodium). Sodium depleted control animals that received 0.9% NaCl as vehicle injected intracerebroventricularly (i.c.v.) ingested 13.0+/-1.5 ml/120 min of 1.8% NaCl. Intracerebroventricular injection of either noradrenaline (80 nmol) or clonidine (20 nmol) inhibited 1.8% NaCl intake from 70 to 90%. Prior i.c.v. injection of diltiazem (6-48 nmol) inhibited from 50 to 100% the effect of noradrenaline and clonidine in a dose-response manner. Diltiazem alone at 100 nmol inhibited, but at 50 nmol had no effect on, sodium appetite. The results suggest: (1) common ionic mechanisms involving calcium channels for the inhibition that noradrenaline and clonidine exert on sodium appetite and (2) a dual role for the benzothiazepine site of L-type calcium channels in the control of sodium appetite.

Isotonic NaCl intake by cell-dehydrated rats.

Male adult rats that received an intragastric load of 2 ml of 12% NaCl (n=13) ingested both water (4.0+/-0.2 ml/2 h) and 0.9% NaCl (3.7+/-1.0 ml/2 h) when compared with rats that received intragastric load of 2 ml of water (water: 0.1+/-0.1; 0.9% NaCl: 0.5+/-0.3 ml/2 h, n=12) in a two-bottle test. Intragastric sodium load increased plasma sodium concentration and osmolality by 5% and reduced plasma renin activity by half compared to rats that received intragastric load of water. Intravenous infusion of 1.5 ml/10 min of 10% NaCl (n=16) also induced ingestion of water (6.2+/-0.8 ml/2 h) and 0.9% NaCl (2.9+/-0.8 ml/2 h) compared with intravenous infusion of 1.5 ml/10 min of 0.9% NaCl (water: 0.9+/-0.4; 0.9% NaCl: 0.5+/-0.2 ml/2 h, n=14). Therefore, a sodium load that raises natremia and plasma osmolality, and therefore induces cell dehydration, results in both 0.9% NaCl and water ingestion when the rats have a two-bottle choice.

Ingestion of hypertonic NaCl vs. palatable drinks by sodium-depleted rats.

This work investigated whether the preference for NaCl solution is shifted to more palatable solutions in the adult male sodium-depleted rat (n=6-10 per group). Animals had daily access to three bottles, one containing water, another 1.8% NaCl (300 mM), and a third containing 0.9% NaCl (150 mM), Gatorade (orange--OG or grape flavored--GG), orange juice (sweetened or unsweetened, from concentrate), or 10% sucrose (no sodium). Sodium content in Gatorade and orange juice ranged from 7 to 14 mEq/l. Daily intakes were recorded for at least 5 days prior to sodium depletion. Then, the animals were depleted of sodium (diuretic plus sodium-deficient diet and water for 24 h). Then, the other two bottles were returned to the animals and the intakes were recorded for 120 min (sodium preference test, SPT). Daily intake from the third bottle (except for unsweetened orange juice) at least doubled the daily 1.8% NaCl intake. The average 1.8% NaCl intake (13+/-2 ml) in the SPT was higher than the intake of 10% sucrose (6+/-1 ml) or of any other solution (less than 6 ml). The intakes of 1.8% NaCl and 0.9% NaCl (10+/-3 ml) were similar during the SPT. The animals also preferred 0.9% NaCl (27+/-1 ml) to OG (3+/-1 ml) in the absence of 1.8% NaCl in the SPT. Therefore, the preference for sodium in sodium-depleted rats also applies when palatable and nutritive solutions are simultaneously available.

Effect of the gadolinium ion on body fluid regulation.

Both osmoreception and baroreception are thought to involve ion channels that are sensitive to changes in membrane stretch. We investigated the effect of a blocker of stretch-activated ion channels, the Gd3+ ion, on osmoregulatory and cardiovascular responses in the intact rat. Intracerebroventricular injection of 50-100 nmol Gd3+ reduced thirst induced by various treatments. Similar doses also reduced intake of saline induced by various treatments. Intracerebroventricular injection of 100 nmol Gd3+ transiently increased arterial pressure and reduced the pressor response to intracerebroventricular angiotensin II (Ang II). Systemic administration of Gd3+ failed to alter thirst, except for a high dose (270 micromol/kg) that induced illness. This high dose failed to prevent urinary hypertonicity and excretion of a load of hypertonic NaCl. Intravenous infusion of 270 micromol/kg of Gd3+ reduced blood pressure and pressure responses to intravenous phenylephrine, but did not reduce the baroreceptor reflex control of heart rate. We conclude that the effects of Gd3+ on thirst and on the cardiovascular system are probably not due to a direct effect of the drug on stretch-sensitive ion channels. Instead, many of the effects of Gd3+ were compatible with blockade of voltage-gated Ca2+ channels.

FURO/CAP: a protocol for sodium intake sensitization.

We investigated if a history of FURO/CAP, a protocol that increases brain angiotensin II (ANG II), sensitizes or enhances sodium intake. A subcutaneous injection of the diuretic furosemide (FURO, 10mg/kg) was combined with a converting enzyme inhibitor captopril (CAP, 5mg/kg) to induce a short latency stimulated sodium (0.3M NaCl) and water intake in a 2h FURO/CAP test. Repeated injections of only FURO/CAP, separated by one-week interval, enhanced stimulated and spontaneous (daily) sodium intake. Stimulated fluid intake was completely suppressed when FURO/CAP was combined with two intraperitoneal injections of the ANG II type-1 receptor antagonist losartan (10, 20, or 40 mg/kg each) given within 1h prior to the FURO/CAP test. Losartan reduced by only 35% the FURO/CAP-induced natriuresis. A history of FURO/CAP, FURO/CAP+losartan (all doses), or vehicle produced similar stimulated fluid intake when all animals received only FURO/CAP in the third final FURO/CAP test. However, a history of vehicle or FURO/CAP+losartan 10mg/kg precluded the enhancement in spontaneous sodium intake after the third final FURO/CAP. The FURO/CAP combined with losartan (all doses) also precluded the spontaneous sodium intake enhancement in the weeks that preceded the third final FURO/CAP test. A history of only FURO/CAP, but not vehicle, also enhanced water deprivation-induced sodium appetite. The results suggest that a history of FURO/CAP enhances stimulated and spontaneous sodium intake, as well as water deprivation-induced sodium appetite, and reinforce the role of ANG II as a peptide that mediates long-term effects on behavior.

Damage to the central amygdala produces differential encephalic c-fos expression in the water deprivation-partial rehydration protocol.

We investigated the effects of electrolytic damage to the central nucleus of the amygdala on brain c-fos expression and 0.3 M NaCl intake of adult male rats (n = 6-12/group) submitted to a cycle of 36 h of water deprivation (WD) followed by 2 h water intake until satiety or partial rehydration (PR). The groups were divided into sham lesion (CEAs), bilateral lesion of the CEA (CEAX) and misplaced lesion with intact CEA (CEAm). The WD-PR produced a marked increase in c-fos expression in the medial parabrachial nucleus (MPBN) and some increase in the parvocelullar portion of the hypothalamic paraventricular nucleus (PVNp), compared to respective hydrated control (no water deprivation) state in CEAX, but not in CEAs or CEAm. The WD-PR induced similar c-fos expression in the lamina terminalis, supraoptic nucleus, magnocellular PVN and lateral parabrachial nucleus in both CEAX and CEAs. The CEAX showed the typical reduced daily need-free 0.3 M NaCl intake compared to CEAs. However, the 0.3 M NaCl intake of CEAX, unexpectedly, was not significantly different from CEAs or intact rats in the sodium appetite test that followed a cycle of WD-PR. The results do not allow associating the alterations in c-fos expression to the typical inhibition of sodium appetite well known in the literature to be produced by damage to the CEA. Nevertheless, the enhanced cell activation in the MPBN and PVNp suggests an inhibitory role for the CEA on the activity of these nuclei when water-deprived rats have quenched their thirst.