P.G. Osborne

Subfornical organ lesion decreases sodium appetite in the sodium-depleted rat.

The effect of subfornical organ (SFO) lesion on various models of ingestive behaviour was investigated in rats. Intake of water after 24 h water deprivation or systemic administration of hypertonic NaCl were not altered by SFO lesions. Intake of food or water after 24 h of food deprivation were not altered by SFO lesions. Intake of NaCl after furosemide-induced Na depletion was decreased by ablation of the SFO. This decrease in Na intake was ameliorated by pretreatment with a low dose of captopril. These results suggest that the SFO is involved in Na intake after Na depletion, but not in water or food intake following periods of water or food deprivation, respectively. The observation that a low dose of captopril can eliminate the decrease in Na appetite which occurred subsequent to SFO lesion suggests that other brain areas may also participate in Na-depletion-induced Na appetite.

Voluntary ethanol intake of individually- or pair-housed rats: Effect of ACTH or dexamethasone treatment

The effect of ACTH or dexamethasone treatment on ingestion of 10% ethanol, 0.5 M NaCl and water was studied in individually- and pair-housed rats. Crowding or decreasing the amount of space per rat by increasing the number of rats per cage from 1 to 2, together with the associated increase in social interactions caused a large increase in ethanol intake. In pair-housed rats and in rats housed alone, ACTH treatment caused a large increase in Na intake but no change in ethanol intake. In pair-housed rats and in rats housed alone, dexamethasone treatment caused no change in either ethanol or Na intake. Thus, it would appear that the induction or maintenance of a high ethanol intake of rats during crowding, a presumed social stressor, can not be attributed entirely to either an increase in blood ACTH levels with the subsequent increase in glucocorticoid hormones or to a decrease in blood ACTH and natural glucocorticoid hormone levels. However, the possibility that ACTH and/or adrenocorticoid hormones, combined with other physiological or environmental factors, causes stressor-induced ethanol intake cannot be excluded.

Effect of variation of the composition of CSF in the rat upon drinking of water and hypertonic NaCl solutions

Infusing conscious unrestrained rats with either 0.5 M NaCl-CSF or 0.7 M sucrose-CSF into the lateral cerebral ventricle (IVT) at 38 microliters/hr for 4 hr induced drinking. Although the infusates were nearly equiosmotic, water drinking during the 0.5 M NaCl-CSF was greater than during 0.7 M sucrose-CSF. However, IVT infusions of 0.7 M mannitol-CSF at rates of 9.4 microliters/hr or 38 microliters/hr for 4 hr or 10 microliters/hr for 4 days failed to induce water drinking. Also, IVT infusion of 0.27 M mannitol-CSF at 38 microliters/hr for 4 hr failed to significantly alter water drinking. CSF [Na] was reduced by IVT infusion of either 0.7 M sucrose-CSF or 0.7 M mannitol-CSF. In contrast, CSF [Na] was increased by 4-hr IVT infusion of 0.5 M NaCl in rats denied access to water during the infusion. Intake of 0.5 M NaCl was not altered significantly from control intakes by any of the above IVT infusions. It is concluded that water drinking in the rat may be initiated by stimulation of either a sodium sensitive sensor alone or with an osmoreceptor system and that species specific differences in the induction of both water drinking and hypertonic saline drinking are apparent.

Inhibition of dehydration induced drinking in rats by reduction of CSF Na concentration

Male rats were dehydrated for 22 h and then given 4 h intracerebroventricular (i.c.v.) infusions which commenced 2 h prior to the beginning of a 2-h fluid access period. I.c.v. infusion of iso-osmotic 0.27 M mannitol-CSF more than halved the amount of water normally drunk by dehydrated rats during the fluid access period. Whilst i.c.v. infusion of 0.7 M mannitol-CSF did not alter the amount of water drunk during the fluid access period. Presumably both infusates reduce CSF [Na] but only 0.7 M mannitol elevates CSF osmolality. The evidence is consistent with the involvement of both sodium and osmoreceptors in thirst in the rat. A reduction of CSF [Na] will inhibit dehydration induced water drinking provided the osmotic pressure of the CSF is not greatly elevated. In addition evidence is provided to show that a contrived reduction of CSF [Na] alone is not a sufficient physiological trigger to initiate salt appetite in rats.

Cerebrospinal fluid pressure of anaesthetized rats during intracerebroventricular infusion

Increases in cerebrospinal fluid pressure (CSFP) were measured in the lateral ventricle in barbiturate anaesthetized male Sprague Dawley rats during intracerebroventricular (IVT) infusions into the contralateral ventricle. IVT infusions of isotonic artificial CSF (art-CSF) solutions at 10 and 38 microliters/hr increased mean CSFP from control preinfusion level of 3.6 cm H2O to 4.6 cm H20 (n.s.) and 5.2 cm H2O (p less than 0.01) respectively with CSFP appearing to attain equilibrium after 30-60 min of infusion. IVT infusion of hyperosmolar art CSF solutions (saccharide and salt solutions of approximate 1000 mOsm/kg) at 38 microliters/hr resulted in a larger increase of CSFP which equilibrated at 8.5 cm H2O (p less than 0.001) after 90 min of infusion. It is suggested that on the basis of CSFP measurements in these and other experiments cited that IVT infusions be run at infusion rates of less than 40 microliters/hr to ensure minimal physiological change.

Decrease of brain extracellular fluid [Na] and its interaction with other factors influencing sodium appetite in sheep

It has been shown previously in sheep that physiological increase of cerebrospinal fluid (CSF) [Na] by infusion of 0.5 M NaCl artificial CSF causes a large reduction of sodium appetite of the sodium-deplete animal. Equivalent increase of CSF osmotic pressure caused by infusion 0.7 M mannitol artificial CSF which lowers CSF [Na] causes a doubling of sodium appetite. The results of the experiments here show that simple dilution of CSF [Na] with isotonic mannitol CSF, as distinct from use of hypertonic 0.7 M mannitol CSF, is an equally effective strong stimulus of sodium appetite. Lowering CSF [Na] concentration stimulates salt appetite in the severely sodium-deplete as well as in the mild to moderately sodium-deplete animal, and the effect of decrease of CSF [Na] on sodium appetite is sustained over 48 h. In addition, i.c.v. infusion of angiotensin II for the preceding 22 h at a rate which is an effective stimulus of both water and sodium solution intake in the sodium-replete animal, in fact, significantly decreased the sodium appetite stimulating effect of reduction of CSF [Na] in the Na-deplete animal.

Effect of varying the composition of CSF on urinary excretion in the conscious rat.

The effect of 4 h intracerebroventricular (i.c.v.) infusion of various solutions on the renal excretion of Na and K and urinary flow rate was examined in conscious unrestrained rats not water-loaded. I.c.v. infusion of iso- or hypo-osmotic solutions with low [Na] induced a diuresis but did not alter renal excretion of Na or K. I.c.v. infusion of hyperosmotic solutions with normal or elevated [Na] induced a natriuresis and kaliuresis. Hyperosmotic mannitol solutions caused a diuresis but hyperosmotic NaCl or sucrose solutions caused a diuresis only when the rats drank water and/or sodium solution during the infusion period. I.c.v. infusion of hyperosmotic NaCl but not hyperosmotic mannitol increased blood pressure. The results are consistent with the involvement of cerebral osmosensors in the control of urinary excretion of Na and K, and of cerebral Na sensors in the control of urinary flow rate. Increased blood pressure, as occurred during i.c.v. infusion of hyperosmotic NaCl, may also contribute to the increased excretion of Na and K.

The role of taste in rapid sodium satiation by sodium-deficient sheep

Sheep with a parotid fistula and sodium-deprived for 24 or 48 h (Na deficit = 500-700 mmol) were trained to drink their entire requirement of sodium bicarbonate solution from a cup in their cage in a single draught for up to 2 min. The cup was connected to a reservoir by an apparatus that enabled the concentration of the solution offered to be changed after the animal had drunk the first 100 or 150 ml of fluid without interrupting the flow of fluid or disturbing the drinking sheep. Under control conditions, the concentrations of solutions in the cup and reservoir were the same, either 900 mM or 300 mM NaHCO3. On experimental days, the concentration of NaHCO3 in the cup and reservoir were different so that the concentration of fluid increased from 300 mM to 900 mM or decreased from 900 mM to 300 mM NaHCO3. On those experimental days when the concentration of NaHCO3 was increased from 300 to 900 mM, the sheep drank a volume of fluid sufficient to maintain intake commensurate with loss. However, when the concentration of NaHCO3 was decreased from 900 to 300 mM, the sheep drank a volume of fluid insufficient to correct the deficit. It is proposed that the failure of sheep to react appropriately to a decrease in NaHCO3 concentration is a consequence of taste adaptation.