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Biomedical subjects

R S Weisinger

Publications and source records attributed to R S Weisinger.

At least 91 records · Page 5Linked to original sources
PubMed1986

Angiotensin and Na appetite of sheep.

The effect of both intravenous (iv; 24 micrograms/h) and intracerebroventricular (ivt; 3.8 micrograms/h) infusion over 1-2 days of angiotensin II (ANG II) on Na intake of both Na-replete and -deplete sheep (i.e., 22 h loss of parotid saliva) was observed. In Na-replete sheep with continuous access to water and 2-h daily access to 0.5 M NaCl solution, both iv and ivt ANG II caused an increase in Na intake. The increase in Na intake caused by iv or ivt ANG II was preceded by a Na deficit due to increased urinary Na excretion. The increase in Na intake was eliminated by the continuous return of urine. In Na-deplete sheep with continuous access to water and 2-h daily access to 0.6 M NaHCO3 solution, iv ANG II caused no change in Na loss but a small increase in Na intake during the 1st day of infusion. The ivt ANG II caused no change in Na loss or in Na intake. The iv ANG II caused a small and inconsistent increase in water intake in Na-replete sheep but did not cause any change in water intake of Na-deplete sheep. The ivt ANG II caused a large increase in water intake in both Na-replete and -deplete sheep. In both Na-replete and -deplete sheep, iv ANG II did not alter cerebrospinal fluid or plasma [Na] or osmolality but decreased plasma [K]. The ivt ANG II decreased both cerebrospinal fluid and plasma [Na] and osmolality. The results of the present experiments are consistent with the proposition that the ANG II-induced Na appetite in sheep is largely due to an ANG II-induced Na loss preceding the development of appetite.

Angiotensin II↗
PubMed1985

Cerebrospinal fluid sodium concentration and salt appetite.

Infusion into a lateral brain ventricle (IVT) of different hypertonic (0.7 M) saccharide solutions decreased [Na+] of cerebrospinal fluid (CSF). Increased Na appetite of moderately Na-deplete sheep was observed during infusion of mannitol, L-glucose or L-fucose, while no change was observed during infusion of D-glucose, D-fucose, D-mannose, 2-deoxy-D-glucose, 3-O-methyl-glucose or fructose. In other experiments, increased Na appetite was observed during infusion of 2.3 mM phlorizin (a relatively specific blocker of Na-coupled glucose transport into cells) or 2.3 mM phlorizin plus 0.7 M D-glucose. In addition, phlorizin eliminated the characteristic decrease in Na appetite but did not affect the increase in water intake caused by IVT infusion of hypertonic NaCl which increased [Na+] of CSF. The results suggest that: (a) there are sensors within the neuropil which respond to change of [Na+] and influence Na appetite, and that these changes of [Na+] are induced deep within the neuropil by those saccharides which do not cross the blood-brain barrier or enter cells; change of CSF[Na+] alone is not sufficient to alter appetite but a change in brain extracellular fluid (ECF)[Na+] is probably necessary; (b) the theory is advanced that the stimulus for altered Na intake could be altered brain ECF[Na+] producing a change in cerebral intracellular fluid (ICF)[Na+] of the sensors; and (c) phlorizin, in reducing or blocking Na-coupled glucose transport, could increase Na appetite by producing a fall in ICF[Na+] of the specific neurones subserving sodium appetite or prevent a decrease in Na appetite caused by IVT infusion of hypertonic NaCl by preventing an increase in ICF[Na+] of this same neuronal system.

Animals↗
PubMed1985

Dehydration-induced sodium appetite in rats.

The effect of 24 hr water deprivation on Na balance was studied in rats. Under baseline conditions, the animals had free access to food and water. During water deprivation, Na excretion was increased, Na intake (i.e., food intake) was decreased and Na deficits of 0.8-1.0 mmol were incurred. During the 24 hr period immediately following the deprivation period when water was returned, Na excretion was decreased and Na balance was restored to baseline or pre-deprivation level. In a second series of experiments, under baseline conditions, the animals had free access to food, water and 0.5 M NaCl. During water deprivation with NaCl solution withheld, Na excretion was not changed relative to baseline but Na deficits of 0.8-1.0 mmol were incurred due to decreased Na intake. During the 24 hr period immediately following deprivation when both water and NaCl solution were returned, intake of the hypertonic NaCl solution was increased and Na balance was restored. In a third series of experiments, under baseline conditions, the animals had free access to food, water, 0.5 M NaCl, 0.5 M KCl, 0.25 M of MgCl2 and 0.25 M CaCl2. During the 24 hr period following water deprivation and also the withholding of the electrolyte solutions, the appetite induced was predominantly for NaCl. The results suggest that the Na appetite observed subsequent to a period of water deprivation may be due to Na deficiency.

Animals↗
PubMed1984

Species differences in the effect of decreased CSF sodium concentration on salt appetite.

During the course of evolution from the beginning of the Caenozoic period, the mammalian species have irradiated into increasingly diverse environments and these physical conditions have imposed powerful selection pressures on the systems of water and salt homeostasis. In the case of physiological actions of hormonal elements of the control systems, effects of antidiuretic hormone and aldosterone on water and salt conservation and of renin-angiotensin II on blood pressure and aldosterone secretion show a general similarity across mammalian species. However, evidence is accruing that there may be large species variation in the vectors of physical, chemical and hormonal changes of the milieu which cause water and salt intake. In the sheep, physiological degree of reduction of CSF [Na] produced by IVT infusion of various hypertonic or isotonic saccharide solutions has a powerful stimulating effect on salt appetite of both Na replete and Na deficient animals. Increasing CSF [Na] reduces appetite. The 0.7 M mannitol CSF infusions initially stimulated thirst but eventually depressed it, presumably due to reduction of CSF [Na]. By contrast, in wild rabbits infusion of 0.9 M mannitol CSF for 2 days at 17 microliter/h caused a large reduction of water intake, a diuresis and no significant increase in salt intake. In laboratory white rats, 0.7 M mannitol CSF infusion at 10 microliter/h for 4 days by Alzet pump, did not increase salt appetite though the infusion was calculated to produce moderate reduction of CSF [Na]. It would appear that there may be significant species differences in effect of reduced CSF [Na] on salt appetite.

Animals↗
PubMed1984

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)

Angiotensin II↗
PubMed1984

The anterior wall of the third cerebral ventricle and homeostatic responses to dehydration.

Within the anterior wall of the third cerebral ventricle, structures are found which have been implicated in the regulation of fluid and electrolyte balance. These structures include the subfornical organ (SFO), preoptic medianus nucleus (PMN) and the organum vasculosum of the lamina terminalis (OVLT). In sheep, the OVLT rises from the ventricular floor over the optic chiasma and occupies most of the midline ventricular wall up to the level of anterior commissure. It contains a plexus of blood vessels at its base which possess fenestrated endothelial cells, and appears to lack ependyma. The SFO of sheep bulges into the third ventricle above the anterior commissure and the PMN is situated between the SFO and OVLT, surrounding the rostral edge of the midline anterior commissure. Like most mammals, water deprivation in sheep results in hypertonicity of body fluids, thirst and graded increase in plasma concentration of vasopressin (AVP). Dehydration also causes a natriuresis in these animals. In sheep with combined ablation of OVLT/PMN tissue, the volume of water drunk, the increases in plasma vasopressin (AVP) level, and the natriuresis in response to dehydration were considerably attenuated, and extreme hypernatremia resulted. Additionally, ablation of OVLT/PMN tissue almost abolished water drinking and AVP secretion in response to systemic infusion of hypertonic NaCl, but did not diminish AVP secretion in response to haemorrhage. In other animals, the OVLT and PMN were individually ablated. While partial osmoregulatory deficits were observed in each case, these deficits were smaller than those observed with combined OVLT/PMN ablation. In contrast to these results, the homeostatic responses to dehydration were not diminished in sheep with combined SFO/PMN lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Cerebral involvement in dehydration-induced natriuresis.

Water deprivation caused daily urinary Na output to more than double in normal sheep, but caused no increase in Na excretion in sheep (A3VL-sheep) in which the anterior third ventricle wall had been ablated. Dehydrated A3VL-sheep exhibited a much greater degree of hypernatremia than dehydrated normal sheep, although water losses were similar in both groups. We postulate that the natriuresis induced by dehydration is a cerebrally mediated homeostatic response.

Animals↗
PubMed1983

Morphology of the organum vasculosum of the lamina terminalis (OVLT) of the sheep.

Examination of the ventricular surface of the organum vasculosum of the lamina terminalis (OVLT) of sheep with the scanning electron microscope revealed an elongated protuberance occupying most of the frontal wall of the third ventricle below the level of the anterior commissure. This protuberance lacked ciliated ependymal cells. Examination of horizontal sections with the transmission electron microscope revealed an apparent lack of regularly apposed ependymal cells, suggesting that ependyma is either greatly modified or absent. The surface was composed of numerous intertwining cell processes with some scattered cells situated on this surface. The body of this structure was composed of many cell processes separated by a network of extracellular channels sometimes extending to the ventricular surface. Towards the base of this protuberance, a plexus of blood vessels was observed. Some of these vessels exhibited fenestrated endothelium. Neuronal processes were also apparent in this region. These unusual anatomical features suggest a specific function for this brain region in sheep.

Animals↗
PubMed1983

Self-administered intravenous infusion of hypertonic solutions and sodium appetite of sheep.

The effects of self-administered iv infusion of hypertonic NaCl, mannitol, glucose, urea, or isotonic NaCl on Na appetite were studied. Sodium-depleted sheep were trained to bar press in order to replace Na deficits of 300-500 mmol. During basal conditions, each delivery to a drinking cup was 15 ml of .6 M NaHCO3 (9 mmol). In the experimental situation, an iv infusion (10 ml) was given automatically with each delivery to the drinking cup. The ingestion of NaHCO3 solution was significantly reduced by all of the hypertonic solutions, the largest decrease being caused by hypertonic NaCl or mannitol. The decreased intake was observed within 10 (with infusion of hypertonic NaCl, mannitol, or glucose) or 20-40 (with urea infusion) min irrespective of whether water was concurrently available to drink. At 20 min, plasma Na concentration was increased by hypertonic NaCl, decreased by mannitol or glucose, and not changed by urea. Cerebrospinal fluid (CSF) Na concentration was increased by all of the hypertonic solutions. Isotonic NaCl had no effect on the ingestion of NaHCO3 solution, plasma, or CSF composition. In regard to the "turn-off" of Na appetite by systemic infusion, these data are consistent with the theory of neural cells within the blood-brain barrier responsive to changes of Na concentration or osmolality in their environment. In contrast, water intake was stimulated by hypertonic NaCl or mannitol but not by urea or glucose, results suggestive that the sensors involved in thirst (e.g., osmoreceptors) are in an area of the brain lacking the blood-brain barrier.

Animals↗
PubMed1983

Lowered cerebrospinal fluid sodium antagonizes effect of raised blood sodium on salt appetite.

Moderately Na-deficient sheep (i.e., Na deficit = 300-400 mmol) will correct their deficit when given hypertonic NaHCO3 solution to drink. Access to NaHCO3 was provided by bar press for 2 h only each day following 22 h of salivary loss from a parotid fistula. Each delivery by bar press provided 9 mmol of NaHCO3 and, of the 46.3 +/- 2.5 deliveries made and drunk in 2 h, 80-90% were made in the first 20 min. Ten minutes before access to NaHCO3 commenced an intracarotid infusion of 4 M NaCl at 1.6 ml/min for 30 min was initiated. This infusion reduced intake by approximately 80% and increased both plasma and cerebrospinal fluid sodium concentration (CSF[Na]). Intraventricular (ivt) infusion of 0.7 M mannitol in artificial CSF at 1 ml/h for 3 h begun 1 h before access to Na by bar press lowered CSF[Na] and approximately doubled voluntary Na intake. The combination of the two procedures resulted in NaHCO3 intake similar to base line. That is, the ivt infusion of 0.7 M mannitol counteracted the inhibition of Na appetite produced by the systemic infusion of hypertonic NaCl, and this was associated with attenuation of the effect of the systemic 4 M NaCl infusion on CSF[Na]. The results suggest that the effects of both the ivt and the systemic infusions are mediated via the same sensor system located within the neuropil.

Animals↗
PubMed1983

Dehydration induces sodium depletion in rats, rabbits, and sheep.

The effect of water deprivation for 1 day on Na balance was measured in rats, rabbits, and sheep. In all three species, dehydration induced a considerable increase in the daily output of Na in urine. This resulted in the water-deprived animals becoming Na depleted as well as water deficient. Experiments were also designed to control for the reduced food intake that results from water deprivation in rats and rabbits. The results showed that decreased food intake was not the cause of the natriuresis and subsequent Na depletion that occurred during dehydration. When water was again made available to the dehydrated animals, a period of urinary Na retention ensued. This Na retention usually continued until the Na deficit that had accrued during the period of dehydration had been ameliorated. It seems likely that natriuresis in response to dehydration is common in mammals. We postulate that such a natriuretic response may serve a homeostatic function in buffering increases in plasma [Na] and osmolality that result from dehydration.

Animals↗
PubMed1982

Osmoregulatory thirst in sheep is disrupted by ablation of the anterior wall of the optic recess.

Ablation of the organum vasculosum of the lamina terminalis (OVLT) and adjacent midline tissue in the anterior wall of the optic recess of the third ventricle resulted in greatly reduced water drinking to intracarotid infusion of hypertonic NaCl in sheep. Daily food and water intake and angiotensin II drinking were not consistently reduced by these lesions. Tissue in or close to the OVLT is probably involved in osmotically induced water-drinking.

Angiotensin II↗
PubMed1982

On the importance of CSF Na in the regulation of renal sodium excretion and renin release.

Infusions (20 microliters/min) of isotonic (0.27 M) mannitol dissolved in Na-free artificial cerebrospinal fluid (CSF) were made for 2 h into the lateral cerebral ventricle (IVT) of conscious 68 h dehydrated sheep. The IVT infusion induced a conspicuous drop in renal sodium excretion and marked rise in plasma renin concentration (PRC). The antinatriuretic response to the IVT infusion was not altered by the intravenous administration of ADH or te converting enzyme blocker (SQ 14225, Captopril). Surgical bilateral renal denervation did not change the antinatriuretic response while the increase in PRC was extinguished. Samples of CSF were collected prior to, and 15 min after the end of the infusion. These showed a reduction in CSF [Na], while CSF osmolality remained unchanged. The study supports the view that sodium sensitive receptors close to the cerebral ventricular system participate in the regulation of renal sodium excretion and renin release, it also suggests that renal sodium excretion is affected by an unknown hormonal factor of cerebral origin, while the release of renin seen in response to a reduction in CSF [Na] is mediated by the renal nerves.

Animals↗
PubMed1982

Role of sodium concentration of the cerebrospinal fluid in the salt appetite of sheep.

The role of sodium concentration of the cerebrospinal fluid (CSF[Na]) in the initiation and/or satiation of Na appetite of Na-deplete or Na-replete sheep was investigated. Slow infusion (1 ml/h) into a lateral brain ventricle of an artificial sheep CSF solution was begun 0-60 min prior to and continued until the end of the Na access period (30-120 min). In Na-deficient sheep, increasing CSF[Na] caused a decrease in Na intake. In both Na-deficient and Na-replete sheep, decreasing CSF[Na] caused an increase in Na intake. The appetite was observed within 25 min of beginning infusion, which represents the most rapid induction of Na appetite yet observed. In Na-replete sheep, the appetite induced by decreasing CSF[Na] was predominantly for Na-containing solutions. A decrease in CSF[Na] of only 4-6 mmol/l was sufficient to induce Na appetite. The results derived by use of different Na, saccharide, or urea containing artificial CSF solutions suggest that there are sensors within the neuropil that respond to change of [Na] and influence salt appetite. They can be accessed by inducing change in [Na] of cerebroventricular CSF.

Animals↗
PubMed1981

Sodium appetite in sheep induced by cerebral ventricular infusion of angiotensin: comparison with sodium deficiency.

Intraventricular administration of supraphysiological amounts of renin, nerve growth factor preparation, or angiotensin II greatly increased the consumption of water and hypertonic sodium bicarbonate solution by sheep. These effects were antagonized by intraventricular administration of drugs that prevent the formation of angiotensin II or block its receptors. The fact that these angiotensin-blocking drugs did not change the sodium intake of sodium-deficient sheep challenges the idea that central angiotensin action is involved in sodium appetite due to a deficiency.

Angiotensin II↗
PubMed1981

Influence of mannitol-induced reduction in CSF Na on nervous and endocrine mechanisms involved in the control of fluid balance.

Infusions (20 microliter/min) of isotonic (0.27 M) and hypertonic (0.7 M) mannitol dissolved in Na-free artificial CSF were made for 1 h. into the lateral cerebral ventricle (IVT) of conscious water-replete sheep. The IVT infusion of both 0.27 M and 0.7 M mannitol induced a water-diuresis. Samples of CSF were collected prior to, and 5, 35, 65, 125 min after the end of the infusion. These consistently showed a reduction in CSF [Na], while CSF osmolality remained unchanged after 0.27 M mannitol, and was considerably increased after 0.7 M mannitol. In the 44 dehydrated sheep IVT infusion of 0.7 mannitol in Na-free artificial CSF was made for 6 h. The water deprivation as such caused a marked increase in plasma and CSF [Na] and osmolality. The 6 h IVT infusion of hypertonic mannitol further increased the CSF osmolality, while CSF [Na] decreased and reached a values below the normal for water-replete animals. The infusion also induced a fall in plasma ADH resulting in a water-diuresis, and extinguished the thirst of the dehydrated sheep. Furthermore, the infusion markedly reduced renal sodium excretion with causing any substantial change in blood aldosterone, in spite of the fact that there was a conspicuous increase in plasma renin concentration. The study supports the view that sodium sensitive receptors close to the cerebral ventricular system participate in the regulation of ADH secretion, water intake, renin release, and renal sodium excretion.

Animals↗