Urinary kallikrein excretion after potassium adaptation in the rat

24-h urinary kallikrein excretion in male Sprague-Dawley rats was measured before and after 14 days with 100 mM potassium chloride as drinking fluid ad libitum. Urinary kallikrein excretion increased in K+-adaptation. The increase was greater when the rats were given distilled water rather than 100 mM sodium chloride to drink prior to the potassium chloride. The urinary potassium excretion increased in all rats studied. The urinary sodium excretion, urine volume and fluid intake increased significantly in rats that had distilled water to drink prior to the KCl. In marked contrast, when rats were offered NaCl prior to KCl, the urinary sodium excretion was unaffected while the urine volume and fluid intake decreased significantly. This study shows that prior NaCl intake abolishes the natriuretic and diuretic effects of KCl load and only suppresses the increase in urinary kallikrein excretion. This suggests that K+ secretory activity at the distal tubules is the major determinant of the release of renal kallikrein in the rat.     

The effect of barbiturates on 24-h water intake and renal excretion of sodium and water in dogs

The effects of barbiturates on 24-h intakes of water and food and urinary excretion of sodium and potassium as well as on plasma concentration of sodium and potassium and osmolality were examined in dogs placed in metabolism cages and fed with a semiliquid diet. Administration of barbiturates stimulated drinking in a Series of 8 dogs having free access to water. Twenty four-h water intake and water balance increased significantly. Food intake, urinary output and urinary excretion of solutes, sodium and water did not change in this Series. A significant decrease in urine output as well as in osmolal clearance and urinary excretion of sodium was observed in a Series of 7 dogs having water restricted for 24 h following administration of barbiturates. Water balance increased in this Series. The same restriction of water in the dogs which had not received barbiturates did not modify renal excretion of water and electrolytes. Plasma osmolality, sodium and potassium concentrations did not change in either Series of experiments. It is concluded that barbiturates induce positive water balance either by stimulation of drinking when water is freely available or by reduction in urine output when water is restricted. The results suggest that expansion of the body fluids following the increased water intake may abolish reduction in urine output and sodium excretion which otherwise occur after administration of barbiturates.     

Effect of various 6-dehydro-corticosteroids, 9, 11-dehydro-DOCA and 9 alpha-fluoro-DOCA on the fluxes of sodium and potassium

The introduction of a double bond at carbons 6 and 7 (6-dehydro-derivatives) of deoxycorticosterone acetate (DOCA), cortisol-21-acetate, 9 alpha-fluorocortisol-21-acetate (9 alpha-F-C-ac) and aldosterone-21-acetate substantially reduces affinity for Type II receptors but not for Type I receptors. Such a modification changes the effect of these steroids on urinary excretion of Na+ and K+. 6-Dehydro-derivatives will thus bind preferentially to receptor Type I inducing the retention of sodium and compete with mineralocorticoids for such receptors. The increase in both natriuresis and kaliuresis when corticosteroids and their 6-dehydro-derivatives are administered together may be interpreted as evidence for a Type II receptor mediation of those ion fluxes. The ionic changes are not mediated by the (Na+ + K+)-ATPase system. The fluoration at 9 and the dehydrogenation at C9C11 of DOCA result in a strong increase of binding to Type I receptor and of sodium retention.     

Differential effects of DOCA on renal and gastrointestinal handling of sodium and potassium in pigs

Young, male pigs eating standard pig chow, ad libitum, received approximately 170 mEq Na and 290 mEq K per day. Electrolyte intake, urinary and fecal electrolyte output, and plasma electrolyte levels were determined daily in 12 deoxycorticosterone acetate (DOCA)-treated pigs and in 6 control pigs. Daily Na and K balances (dietary intake - urinary + fecal output) were calculated. DOCA caused a reduction in urinary Na output from 1.53 mEq/kg/day to 0.57 mEq/kg/day during the first 48 hr following implantation. Escape from the renal sodium retaining effect of DOCA was complete within 3 days, with urinary Na output returning to pre-DOCA levels. Fecal Na output decreased from 0.65 mEq/kg/day during the preimplant period to 0.13 mEq/kg/day during the postimplant period. No escape from GI Na retention occurred by Day 15. Plasma Na rose to significantly higher levels by Day 15. Sodium balance was significantly elevated in DOCA-treated pigs for that first 48 hr postimplant. Urinary K output decreased from 3.50 mEq/kg/day to 1.74 mEq/kg/day during the first 2 days, but returned toward preimplant levels by Day 4. Fecal K output was increased for the first week, and thereafter returned to preimplant levels. Plasma K fell from 3.9 to 2.9 mEq/liter by Day 15. Potassium balance fell slightly in both experimental and control animals. No significant differences in potassium balance were present between the two groups. The control pigs showed no significant changes in plasma electrolyte concentration or in electrolyte balance. It is concluded that DOCA has differential effects on renal and gastrointestinal handling of electrolytes and that DOCA may induce an intracellular shift of potassium in pigs.     

Water and electrolyte excretion during the oestrous cycle in sheep.

Electrolyte excretion was observed during 24 oestrous cycles in housed sheep, together with mixed salivary Na/K ratio during 10 additional cycles. 1. The sharp fall in food and fluid intake at oestrus accompanied a peak of sodium excretion which changed to peak retention 3 days later, both in faeces and urine. 2. Potassium excretion declined with food intake at oestrus but subsequently failed to recover to pre-oestrous levels dispite full recovery of dietary intake. 3. Curiously, water intake also recovered completely whereas urinary and faecal water retention continued; faecal loss actually exceeded renal excretion on these liberal water intakes. 4. Changes in salivary, urinary and faecal Na/K indicated an aldosterone peak neither during the luteal phase nor at oestrus but three days later. The data raise questions concerning the regulation of water and electrolyte balance within the normal cycle. They also provide a baseline for the investigation of renal effects of gonadal steroids. Possible roles for aldosterone, ADH and progesterone in maintaining fluid and electrolyte balance are discussed, emphasising problems confronting species which have evolved with heavy obligatory potassium excretion but undependable supplies of sodium and water.     

Fecal Selenium Excretion Is Regulated by Dietary Selenium Intake

Whole-body selenium is regulated by excretion of the element. Reports of studies carried out using isotopic tracers have led to the conclusion that urinary selenium excretion is regulated by selenium intake but that fecal excretion is not. Because of the limitations of tracer studies, we measured urinary and fecal selenium excretion by mice with selenium intakes in the form of sodium selenite ranging from deficient to almost toxic. Tissue and whole-body selenium concentrations increased sharply between deficient and adequate selenium intakes, reflecting tissue accumulation of selenium in the form of selenoproteins. Once the requirement for selenium had been satisfied, a 31-fold further increase in intake resulted in less than doubling of tissue and whole-body selenium, demonstrating the effectiveness of selenium excretion by the mouse. Urinary selenium excretion increased with increases in dietary selenium intake. Fecal selenium excretion, which was 20 to 30?% of the selenium excreted in the physiological range, responded to moderately high selenium intake but did not increase further when selenium intake was increased to even higher levels. Thus, fecal selenium excretion contributes to regulation of whole-body selenium at physiological selenium intakes. The pattern of its response to the full spectrum of selenium intakes was different from the urinary excretion response, suggesting that the mechanisms of fecal and urinary routes of excretion are different.     

Electrolyte balance, mode of delivery and plasma aldosterone levels in newborn lambs

Plasma aldosterone, sodium (Na) and potassium (K) concentrations, daily Na and K intakes, and urinary and faecal excretion were measured during the first week of postnatal life in 9 lambs naturally born at term (145 days of gestation) and in 10 lambs delivered by caesarean section on day 145 (6 lambs) or on day 139 (4 lambs) of gestation. Plasma aldosterone, Na and K concentrations showed no significant variation during the experimental period in any group of lambs, and there was no significant difference concerning these parameters among the three groups. Na and K balances were always positive during the experimental period in naturally born lambs. It was negative on days 4 and 6 postdelivery in those delivered by caesarean section on days 145 and 139 of gestation, respectively. This was probably due to the lower daily Na and K intakes measured in these 10 lambs compared to the 9 control lambs: urinary output and urinary Na and K excretion were lower in the two groups of lambs delivered by caesarean section, while Na and K urinary concentrations were not different in any group.     

Effect of high and low sodium intake on urinary aquaporin-2 excretion in healthy humans

The degree of water transport via aquaporin-2 (AQP2) water channels in renal collecting duct principal cells is reflected by the level of the urinary excretion of AQP2 (u-AQP2). In rats, the AQP2 expression varies with sodium intake. In humans, the effect of sodium intake on u-AQP2 and the underlying mechanisms have not previously been studied. We measured the effect of 4 days of high sodium (HS) intake (300 mmol sodium/day; 17.5 g salt/day) and 4 days of low sodium (LS) intake (30 mmol sodium/day; 1.8 g salt/day) on u-AQP2, fractional sodium excretion (FE(Na)), free water clearance (C(H2O)), urinary excretion of PGE(2) (u-PGE(2)) and cAMP (u-cAMP), and plasma concentrations of vasopressin (AVP), renin (PRC), ANG II, aldosterone (Aldo), atrial natriuretic peptide (ANP), and brain natriuretic peptide (BNP) in a randomized, crossover study of 21 healthy subjects, during 24-h urine collection and after hypertonic saline infusion. The 24-h urinary sodium excretion was significantly higher during HS intake (213 vs. 41 mmol/24 h). ANP and BNP were significantly lower and PRC, ANG II, and Aldo were significantly higher during LS intake. AVP, u-cAMP, and u-PGE(2) were similar during HS and LS intake, but u-AQP2 was significantly higher during HS intake. The increases in AVP and u-AQP2 in response to hypertonic saline infusion were similar during HS and LS intake. In conclusion, u-AQP2 was increased during HS intake, indicating that water transport via AQP2 was increased. The effect was mediated by an unknown AVP-independent mechanism.     

Effect on maternal and fetal renal function and plasma renin activity of a high salt intake by the ewe

The effect on renal function of replacing maternal drinking water with a solution containing 0.17 M NaCl was studied in 9 ewes and their chronically catheterised fetuses over a period of 9 days. Maternal sodium intake increased from control values of 2.19 +/- 0.09 mmol/h to 44.3 +/- 7.4 (P less than 0.001) and 46.3 +/- 6.5 mmol/h (P less than 0.001) on the 3rd and 6th days of salt ingestion. Maternal plasma sodium levels were not affected, but the urinary sodium/potassium ratio increased from 0.15 +/- 0.07 to 2.26 +/- 0.34 (P less than 0.001) after 6 days and plasma renin activity fell from 2.87 +/- 0.76 to 1.00 +/- 0.25 ng/ml per h (P less than 0.05). The changes in maternal sodium intake had no effect on fetal plasma sodium levels nor on fetal plasma renin activity. Sodium excretion and fetal urinary sodium/potassium ratio did not change. However, 3 days after the ewes returned to drinking water fetal plasma renin activity was significantly higher than it was prior to maternal ingestion of 0.17 M NaCl. Fetal plasma renin activity was inversely related to fetal plasma sodium levels (P less than 0.01). The results show that changes in maternal sodium intake had no long term effect on fetal plasma sodium levels nor on fetal renal sodium excretion. The fall in maternal plasma renin activity in the absence of any change in the fetal renin activity, indicates that the fetal renin angiotensin system is controlled by factors other than those influencing the maternal renin angiotensin system. Since fetal urinary sodium/potassium ratios remained unchanged it would suggest that fetal sodium excretion is not influenced by maternal levels of aldosterone.     

Mineralocorticoid treatment attenuates activation of oxytocinergic and vasopressinergic neurons by icv ANG II

Central oxytocin (OT) neurons limit intracerebroventricular (icv) ANG II-induced NaCl intake. Because mineralocorticoids synergistically increase ANG II-induced NaCl intake, we hypothesized that mineralocorticoids may attenuate ANG II-induced activation of inhibitory OT neurons. To test this hypothesis, we determined the effect of deoxycorticosterone (DOCA; 2 mg/day) on icv ANG II-induced c-Fos immunoreactivity in OT and vasopressin (VP) neurons in the supraoptic (SON) and paraventricular (PVN) nuclei of the hypothalamus and also on pituitary OT and VP secretion in male rats. DOCA significantly decreased the percentage of c-Fos-positive (%c-Fos+) OT neurons in the SON and PVN, both in the magnocellular and parvocellular subdivisions, and the %c-Fos+ VP neurons in the SON after a 5-ng icv injection of ANG II. DOCA also significantly reduced the %c-Fos+ OT neurons in the SON after 10 ng ANG II and tended to attenuate 10 ng ANG II-induced OT secretion. However, the %c-Fos+ OT neurons in DOCA-treated rats was greater after 10 ng ANG II, and DOCA did not affect the %c-Fos+ OT neurons in the PVN nor VP secretion or c-Fos immunoreactivity in either the SON or PVN after 10 ng ANG II. DOCA also did not significantly alter the effect of intraperitoneal (ip) cholecystokinin (62 microg) on %c-Fos+ OT neurons or of ip NaCl (2 ml of 2 M NaCl) on the %c-Fos+ OT and VP neurons. These findings indicate that DOCA attenuates the responsiveness of OT and VP neurons to ANG II without completely suppressing the activity of these neurons and, therefore, support the hypothesis that attenuation of OT neuronal activity is one mechanism by which mineralocorticoids enhance NaCl intake.     

Potentiated effect of systemic administration of oxytocin on hypertonic NaCl intake in food-deprived male rats

Subcutaneous administration of oxytocin (OT) increases water intake and sodium/urine excretion in food-deprived male rats. This study analyzes the effect of OT administration (at 0830 and 1430h) on the consumption of water and hypertonic NaCl (1.5%). In the first experiment, injections of OT increased the intake of hypertonic NaCl (but not of water) in food-deprived rats but not in ad lib-fed animals during the second 12 h (2030 to 0830) of the treatment day. The net concentration of the fluid consumed by OT/deprived animals was close to isotonic. In the second experiment, the initial effect of OT administration was an increase in urine volume and urinary sodium excretion and concentration by food-deprived animals during the first 12 h (0830 to 2030). These findings suggest that in food-deprived animals, systemic administration of OT induces NaCl intake as a consequence of previous urine loss and urinary sodium excretion.     

Hypertensinogenic factors and renal alpha-adrenoceptors in young SHR and WKY rats

The effects of high sodium intake (drinking 1% NaCl), DOCA and DOCA + 1%NaCl for 6 weeks on renal alpha 1- and alpha 2-adrenoceptors and on systolic blood pressure (SBP) were examined in young spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). On normal sodium intake, SHR rats had higher renal alpha 1 (p less than .001) and alpha 2-adrenoceptor densities (p less than .001) and SBP (p less than .001) than WKY rats. Although, WKY rats given either 1% NaCl, DOCA, and DOCA + 1% NaCl developed hypertension after 6 weeks of treatment, only 1% NaCl administration for the same period produced an increase in the alpha 1- and alpha 2-adrenoceptor densities when compared to the control (p less than .01 and p less than .001, respectively). In the SHR rats, to the contrary, ingestion of 1% NaCl and DOCA + 1% NaCl increased the already elevated alpha 2-adrenoceptor density (p less than .001) and SBP even more in this strain after 6 weeks of treatment. Equilibrium dissociation constants (KD), however, were similar for both classes of receptors in experimental and control rats. This study indicates that postweaning exposure of the WKY and SHR rats to a high salt treatment and DOCA can influence the renal alpha-adrenoceptor densities. Although the functional significance of the changes is unclear, it is reasonable to speculate that postweaning exposure to a hypertensinogenic stimuli such as a 1% NaCl and/or DOCA may ultimately interfere with the functional development of the kidney differently in rats genetically predisposed to hypertension (SHR) from normotensive (WKY) rats.     

Biological half-life of bromide in the rat depends primarily on the magnitude of sodium intake

The parallel course of the excretion rates of bromide and sodium ions was demonstrated in adult male and female rats administered simultaneously with potassium 82Br-bromide and 24Na-sodium chloride. The animals were exposed to various intakes of sodium ions accompanied with five different anions: Br-, Cl-, HCO3-, ClO4-, and SCN-. Regardless of the anion accompanying the sodium ion, the excretion rates of 82Br- and 24Na+ ions were proportional to the magnitude of sodium intake in the animals. Hence, we have proved our hypothesis that the biological half-life of bromide depends on the magnitude of sodium intake rather than on the intake of chloride.     

Altered regulation of renal sodium transporters and natriuretic peptide system in DOCA–salt hypertensive rats

Although deoxycorticosterone acetate (DOCA)–salt hypertension is a volume dependent model of hypertension, it shows polyuria and natriuresis. It is expected that dysregulation of aquaporin water channels (AQPs) and sodium transporters associated with natriuretic peptide (NP) system may play an escape role in sodium retaining state. One week after left unilateral nephrectomy, rats were subcutaneously implanted with silastic DOCA (200 mg/kg) strips. Physiologic saline was supplied as a drinking water to all animals. 4 weeks after operation, the protein expression of AQPs, sodium transporters, and endopeptidase (NEP) was determined in the kidneys by semiquantitative immunoblotting and immunohistochemistry. The mRNA expression of NP system was determined by real-time polymerase chain reaction. The amount of urinary ANP excretion was measured by radioimmunoassay. In DOCA–salt rats, urine osmolality was decreased while urinary excretion of sodium was increased. The expression of AQP1-3 as well as that of α-1 subunit of Na,K–ATPase, NHE3, NKCC2 and NCC was decreased in the kidney. The mRNA expression of ANP, brain natriuretic peptide (BNP), C-type natriuretic peptide (CNP) was increased in the kidney. The expression of NEP was decreased, and urinary ANP excretion was increased. Downregulation of AQPs and sodium transporters may contribute to mineralocorticoid escape in DOCA–salt hypertension. Increased expression of natriuretic peptides associated with downregulation of NEP may play a role in natriuresis.     

Effect of acarbose on the increased plasma concentration of uric acid induced by sucrose ingestion

Sucrose is converted fructose and glucose, which may increase plasma uric acid concentration (pUA) through increased purine degradation and/or decreased uric acid (UA) excretion. To investigate effects of acarbose, an inhibitor of alpha-glucosidase, on the increased pUA from sucrose administration, we measured pUA and urinary UA excretion in 6 healthy subjects before and after administering sucrose, with and without co-administration of acarbose. Sucrose raised pUA by 10% (p < 0.01). However, excretion and fractional clearance of UA were unchanged. Sucrose and acarbose coadministration also increased pUA, but less than did sucrose alone (sucrose: 4.9 to 5.4 mg/dl; sucrose + acarbose, 4.7 to 4.9 mg/dl, p < 0.05) without changes in urinary excretion and fractional clearance of UA. Acarbose appears to attenuate the rise in pUA by sucrose ingestion by inhibiting sucrose absorption.     

Effects of fresh and seawater ingestion on osmoregulation in Atlantic bottlenose dolphins (Tursiops truncatus)

Bottlenose dolphins (Tursiops truncatus) are marine mammals with body water needs challenged by little access to fresh water and constant exposure to salt water. Osmoregulation has been studied in marine mammals for a century. Research assessing the effects of ingested fresh water or seawater in dolphins, however, has been limited to few animals and sampling times. Nine 16- to 25-h studies were conducted on eight adult dolphins to assess the hourly impact of fresh water, seawater, and seawater with protein ingestion on plasma and urine osmolality, urine flow rate (ufr), urinary and plasma solute concentrations, and solute clearance rates. Fresh water ingestion increased ufr. Fresh water ingestion also decreased plasma and urine osmolality, sodium and chloride urine concentrations, and solute excretion rates. Seawater ingestion resulted in increased ufr, sodium, chloride, and potassium urine concentrations, sodium excretion rates, and urine osmolality. Seawater with protein ingestion was associated with increased ufr, plasma osmolality, sodium excretion, and sodium, chloride, potassium, and urea urine concentrations. In conclusion, bottlenose dolphins appear to maintain water and plasma solute balance after ingesting fresh water or seawater by altering urine osmolality and solute clearance. Ingestion of protein with seawater appears to further push osmoregulation limits and urine solute concentrations in dolphins.     

Effects of hypotension and fluid depletion on central angiotensin-induced thirst and salt appetite

We examined the effects of hypotension and fluid depletion on water and sodium ingestion in rats in response to intracerebroventricular infusions of ANG II. Hypotension was produced by intravenous infusion of the vasodilator drug minoxidil (25 microg x kg(-1) x min(-1)) concurrently with the angiotensin-converting enzyme inhibitor captopril (0.33 mg/min) to prevent endogenous ANG II formation. Hypotension increased water intake in response to intracerebroventricular ANG II (30 ng/h) but not intake of 0.3 M NaCl solution and caused significant urinary retention of water and sodium. Acute fluid depletion was produced by subcutaneous injections of furosemide (10 mg/kg body wt) either alone or with captopril (100 mg/kg body wt sc) before intracerebroventricular ANG II (15 or 30 ng/h) administration. Fluid depletion increased water intake in response to the highest dose of intracerebroventricular ANG II but did not affect saline intake. In the presence of captopril, fluid depletion increased intakes of both water and saline in response to both doses of intracerebroventricular ANG II. Because captopril administration causes hypotension in fluid-depleted animals, the results of the two experiments suggest that hypotension in fluid-replete animals preferentially increases water intake in response to intracerebroventricular ANG II and in fluid-depleted animals increases both salt and water intake in response to intracerebroventricular ANG II.     

Handling of water and dietary monovalent ions by the young turkey

Sodium and water turnover rates were measured in young turkeys fed diets with three concentrations of NaCl and kept at 12, 18 or 30 degrees C. Sodium absorption averaged approximately 60% and was unaffected by temperature. Water and sodium pools were affected by temperature and sodium intake. Water turnover was linear to sodium turnover at the lower two temperatures. No significant relationship was apparent in birds kept at 30 degrees C. The reciprocal of the slope of the function of water turnover on sodium turnover was 125-170 mM, suggesting an increase in isotonic urine excretion with sodium intake and a corresponding increase in water intake. Dietary sodium and potassium stimulated water turnover similarly. Dietary chloride concentration did not affect water turnover. In the turkey plasma pH and pCO2 were unaffected by a wide range of the anion-cation balance. It is concluded that excess sodium or potassium intakes is handled effectively in the turkey by increased water intake and excretion.     

AT(1) receptor blockade with losartan during gestation in Wistar rats leads to an increase in thirst and sodium appetite in their adult female offspring

We studied the effects of angiotensin II receptor blockade with losartan on thirst and sodium appetite in pregnant Wistar rats and on their adult female offspring. During maternal adaptation to pregnancy, average daily total water intake increased by 63% (P<0.01); NaCl intake by 214% (P<0.001). These changes were not blocked by daily s.c. injections of losartan (50 mg/kg bw i.p.) from gestation day (GD) 2 until GD 19 which implied that maternal AT(1) receptors were not involved in the up regulation of thirst and sodium appetite during pregnancy. Losartan blockade during gestation led to a significant and continued increase in thirst and sodium appetite in the adult female offspring. Daily water intakes were greater in the losartan (LO) group than in the vehicle-injected control group (CO), leading to a total water intake of 1114 +/- 80.6 ml/kg bw compared with 738 +/- 56.7 ml/kg bw (P<0.05) during the 8-day period of observation. Daily sodium intakes were usually 2-3 times greater in the LO group compared with the CO group, amounting to a final cumulative intake of 232 +/- 33 mmol/kg bw compared with 93.8 +/- 16.5 mmol/kg bw (P<0.05) in 8 days. These elevated sodium and water intakes were nearly counterbalanced by the increased renal excretion of water and sodium by fully functional kidneys that were not injured by the drug. Body weights were 10% lower in the LO group at the start but remained unchanged relative to the CO group during the entire 8-day period of observation. Plasma electrolytes, blood hematocrit and carotid MABP in the LO group did not differ from the CO group.     

What makes wild rabbits drink?

Wild rabbits Oryctolagus cuniculus (L) introduced to Australia over a century ago successfully colonized diverse environments in a large part of the continent varying from arid desert, alps, to lush grasslands and coastline where water and salt may be either abundant or very scarce. Wild rabbits caught in Northern Victoria were studied under laboratory conditions, where they adapted to dry pelleted food and drank regularly water and a cafeteria of electrolyte solutions offered. Intracerebroventricular (IVT) infusion of angiotensin II (AII) in doses 10, 50 and 500 ng/h did not increase their water drinking, but increased salt appetite, although it was delayed one or more days after the beginning of AII infusion. IVT infusion of AII 500 ng/h for one day caused a halving in water intake and a tenfold increase in sodium excretion. These were followed by compensatory changes in water and 0.5 M NaCl intake on the consecutive days. IVT infusion of AII 50 ng/h for one day induced an increased urinary sodium excretion, a negative sodium balance which was not followed by an increased salt appetite. IVT infusion of AII 10 ng/h for five days caused a progressive increase in sodium excretion and salt appetite which were significant on the fourth day of infusion and both remained eight-ten times greater than control levels for three days after the cessation of infusion. Water intake was unchanged. IVT infusion of 0.3 M Na-CSF for two days reduced water and food intake, and caused a negative sodium balance on the second day of infusion which was not followed by increase in salt appetite.(ABSTRACT TRUNCATED AT 250 WORDS)