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PubMed1987

Sugar uptake by fluid-phase pinocytosis and diffusion in isolated rat hepatocytes.

Measurements of sugar pinocytosis (fluid-phase endocytosis of radiolabelled sucrose, lactose and raffinose) in freshly isolated rat hepatocytes are disturbed by sugar diffusing into the cells through plasma-membrane blebs. Non-pinocytic entry may be even more pronounced at 0 degrees C, and is a major contributor to 'background' radioactivity. By electrodisruption of the plasma membrane, a distinction can be made between pinocytotically sequestered sugar and free sugar that has entered the cytosol by diffusion. Pinocytosis proceeds at a rate of 2%/h (relative to the intracellular fluid volume), whereas the rate of sucrose entry by diffusion is more than twice as high. Three pinocytotic compartments are distinguishable in isolated hepatocytes: (1) a rapidly recycling compartment, which is completely destroyed by electrodisruption, and which may represent pinocytic channels continuous with the plasma membrane; (2) a non-recycling (or very slowly recycling) electrodisruption-resistant compartment, which allows accumulation of the lysosomally hydrolysable sugar lactose, and which therefore must represent non-lysosomal vacuoles (endosomes?); (3) a lysosomal compartment (non-recycling, electrodisruption-resistant), which accumulates raffinose and sucrose, but which hydrolyses lactose. The last two compartments can be partially resolved in metrizamide/sucrose density gradients by the use of different sugar probes.

Animals↗
PubMed1971

Effect of ca on the synthesis of deoxyribonucleic Acid in virulent and avirulent yersinia.

Virulent and potentially virulent cells of Yersinia (Pasteurella) pestis produce virulence or V and W antigens (VW(+)) but remain static at 37 C during aeration in enriched Ca(2+)-deficient media containing 0.02 m Mg(2+). In this environment, which simulates mammalian intracellular fluid, VW(+) cells possessed a functional cytoplasmic membrane as judged by concentration of (14)C-isoleucine, release of (32)P, and consumption of oxygen at rates comparable to those of dividing cells cultivated with Ca(2+). Furthermore, rates of protein and ribonucleic acid synthesis were essentially identical in dividing and static VW(+) cells and in mutant VW(-) organisms. However, the rate of deoxyribonucleic acid (DNA) synthesis in static cells was about 10% of that observed in dividing organisms. Accordingly, bacteriostasis of VW(+) cells in the simulated intracellular environment is evidently caused by reactions directly associated with cessation of DNA synthesis rather than by alterations in the regulatory capacity of the cytoplasmic membrane.

Journal Article↗
PubMedDate not supplied

A physiological analysis of hyponatremia: implications for patients on peritoneal dialysis.

The basis for hyponatremia is a negative balance for sodium (Na+) plus potassium (K+) and/or a positive balance for water. In patients with normal renal function, vasopressin is needed to prevent the excretion of electrolyte-free water. Vasopressin is not important when there is little residual renal function. If hyponatremia is accompanied by a quantitatively appropriate gain in weight, this implies that a gain of electrolyte-free water was the basis for hyponatremia. In the absence of this weight gain, a loss of salts is to be suspected. If the extracellular fluid (ECF) volume is obviously low, hyponatremia is due to a deficit of NaCl, unless there is a deficit of K+. With a KCl deficit and a contracted ECF volume, there should also be a large shift of Na+ into cells, so metabolic alkalosis would not be an expected finding. In contrast, those patients with no change in weight who have a normal or expanded ECF volume are subdivided into those with a gain of solutes restricted to the ECF compartment (glucose, mannitol), or those with a deficit of solutes of intracellular fluid origin, which implies that a catabolic state (malnutrition) may be present.

Extracellular Space↗
PubMed1989

Serum beta 2 microglobulin and extracellular fluid volume during haemodialysis.

Conflicting results have been published concerning serum beta 2 microglobulin (beta 2-M) kinetics during dialysis with a cuprophane membrane which is not permeable for the protein. We have investigated the hypothesis that the apparent increase of free serum beta 2-M could result from extracellular fluid volume (ECV) contraction. Using inulin, ECV was measured before and 1 h after a dialysis session with a sodium dialysate concentration of 145 mmol/l. Dialysis was performed either with a cuprophane or a high-flux membrane. Transcellular water shift and changes in beta 2-M concentration were calculated from total body water changes (ultrafiltration) and ECV. ECV decreased from a predialysis value of 16.6 +/- 3.51 (mean +/- SD) (24.9% bodyweight) to a postdialysis value of 11.9 +/- 2.11 (19.8% bodyweight). Ultrafiltration was only 3.1 +/- 1.01, indicating concomitant water shift from ECV to intracellular fluid space. A significant decrease in corrected beta 2-M concentration was found for high-flux membranes. However, postdialysis beta 2-M did not change significantly after dialysis with cellulosic membranes. In conclusion, the apparent increase of serum beta 2-M concentration measured during dialysis with cellulosic membranes may be explained by ECV contraction. These results have to be taken into account for any pathogenic mechanism of the beta 2-M-associated amyloidosis occurring in long-term haemodialysed patients.

Amyloidosis↗
PubMed1985

Cortisol kinetics and fluid distribution in brook trout (Salvelinus fontinalis).

Cortisol kinetics were examined in brook trout (Salvelinus fontinalis) to assess possible relationships with body fluid distribution during acclimation to sea water (SW). The disappearance curve of [3H]cortisol in plasma, after a bolus injection, was analysed by compartmental analysis using a three-pool mammillary model. The results indicated that only approximately 10% of the total exchangeable cortisol was located in the plasma pool. Over 75% of the total cortisol was associated with a large slowly exchanging pool and the remaining cortisol was located in a second extravascular tissue pool which was in rapid exchange with the plasma pool. Two days after transfer of trout from fresh water to SW, when plasma chloride concentration was at a new steady state, body weight, intracellular fluid volume, haematocrit and inulin clearance rate were lowered but plasma, blood and extracellular volumes were unaltered. Cortisol plasma clearance rate was unaltered but plasma cortisol concentration, cortisol secretion rate, total cortisol pool size and interpool transport rates were increased. These results are consistent with an acute role for cortisol in SW adaptation of brook trout. The fraction of the total cortisol cleared was smaller and the average time that cortisol spent in the tissue pools was slightly longer in trout after transfer to SW, possibly reflecting altered fluid dynamics. The fractional disappearance rate was larger at higher plasma cortisol concentrations in the SW trout. This relationship is compatible with the hypothesis that cortisol protein binding protects cortisol from metabolism.

Adaptation, Physiological↗
PubMed2005

Extracellular and intracellular acid-base status with regard to the energy metabolism in the oyster Crassostrea gigas during exposure to air.

The acid-base status of extra- and intracellular fluids was studied in relation to the anaerobic energy metabolism in the adductor muscle, mantle, gills, and heart of the marine bivalve Crassostrea gigas after exposure to air for periods of 2, 4, 8, 12, 24, and 48 h. Such exposure was found to cause a significant reduction in the pH in the hemolymph (pH(e)) within the first 4 h. The decrease in the pHe was accompanied by elevated Pco2 values, causing [HCO3-] to rise (respiratory acidosis). Thereafter, the pHe fell at a lower rate, and this fall was partially compensated for by a further increase in [HCO3-] in the hemolymph. The increase in the [Ca] levels in the hemolymph indicates a mobilization of Ca2+ from CaCO3 and the involvement of bicarbonates in the buffering of pHe. The main anaerobic end-products that accumulated in the tissues during the first stages of anaerobiosis were alanine and succinate, at a ratio of about 2 : 1. Later on, propionate and acetate were also accumulated at significant rates. In contrast to the adductor muscle, gills, and mantle, opine production in the heart was significant after 12-24 h of exposure to air. Determination of intracellular pH (pHi) revealed that there is a close relationship between the rate of anaerobic end-product accumulation and the extent of intracellular acidosis in the adductor muscle, mantle, and gills. On the contrary, accumulation of anaerobic end-products in the heart did not cause any significant change in its pHi. The intracellular nonbicarbonate, nonphosphate buffering value (beta (NB,NPi)) was determined to be higher in the heart than in the other three tissues and thus probably plays a crucial role in stabilizing heart pHi during exposure to air.

Acid-Base Equilibrium↗
PubMedDate not supplied

Pathomechanisms of cystoid macular edema.

Cystoid macular edema (CME) is a well-known endpoint of various ocular diseases, but the relative pathogenic impact of extra- and intracellular fluid accumulation within the retinal tissue still remains uncertain. While most authors favor an extracellular fluid accumulation as the main causative factor of cyst formation, there are indications that Müller cell swelling may also contribute to CME development (particularly in cases without significant angiographic vascular leakage). Vascular leakage occurs after a breakdown of the blood-retinal barrier during traumatic, vascular, and inflammatory ocular diseases, and allows the serum to get into the retinal interstitium. Since intraretinal fluid distribution is restricted by two diffusion barriers, the inner and outer plexiform layers, serum leakage from intraretinal vessels causes cysts mainly in the inner nuclear layer while leakage from choroid/pigment epithelium generates (in addition to subretinal fluid accumulation) cyst formation in the Henle fiber layer. In the normal healthy retina, the transretinal water fluxes are mediated by glial and pigment epithelial cells. These water fluxes are inevitably coupled to fluxes of osmolytes; in the case of glial (Müller) cells, to K(+) clearance currents. For this purpose, the cells express a complex, microtopographically optimized pattern of transporters and channels for osmolytes and water in their plasma membrane. Ischemic/hypoxic alterations of the retinal microvasculature result in gliotic responses which involve down-regulation of K(+) channels in the perivascular Müller cell end-feet. This means a closure of the main pathway which normally generates the osmotic drive for the redistribution of water from the inner retina into the blood. The result is an intracellular K(+) accumulation which, then, osmotically drives water from the blood into the glial cells (i.e., in the opposite direction) and causes glial cell swelling, edema, and cyst formation. While the underlying mechanisms await further research, it is expected that their improved knowledge will stimulate the development of novel therapeutic approaches to resolve edema in retinal tissue.

Blood-Retinal Barrier↗
PubMed2001

Magnitude and variation of ratio of total body potassium to fat-free mass: a cellular level modeling study.

Potassium is an essential element of living organisms that is found almost exclusively in the intracellular fluid compartment. The assumed constant ratio of total body potassium (TBK) to fat-free mass (FFM) is a cornerstone of the TBK method of estimating total body fat. Although the TBK-to-FFM (TBK/FFM) ratio has been assumed constant, a large range of individual and group values is recognized. The purpose of the present study was to undertake a comprehensive analysis of biological factors that cause variation in the TBK/FFM ratio. A theoretical TBK/FFM model was developed on the cellular body composition level. This physiological model includes six factors that combine to produce the observed TBK/FFM ratio. The ratio magnitude and range, as well as the differences in the TBK/FFM ratio between men and women and variation with growth, were examined with the proposed model. The ratio of extracellular water to intracellular water (E/I) is the major factor leading to between-individual variation in the TBK/FFM ratio. The present study provides a conceptual framework for examining the separate TBK/FFM determinants and suggests important limitations of the TBK/FFM method used in estimating total body fat in humans and other mammals.

Adipose Tissue↗
PubMed1982

51Cr EDTA determinations of the extracellular fluid volume in hemorrhage: a study with fed and starved rats.

Extracellular fluid volumes have been determined in fed and 24-30 h starved rats, before and after 60 min of hemorrhagic hypotension at 70 mmHg. Bilateral renal vascular ligation was carried out to prevent clearance of the isotope tracer used, 51Cr EDTA. The time taken for a bolus of the tracer to distribute itself in its space, was determined in fed and starved animals after the standard period of hypotension. This was found to be 37 min for fed animals, and 50 min for those which had been starved. When the isotope ECF space was compared before and after hemorrhage in fed animals, it was unchanged, despite an estimated blood volume loss of 39%. The isotope ECF space was reduced 5.5% after hemorrhage in animals which had been starved. It is concluded that fed rats mobilised intracellular fluid to the interstitium in hemorrhage, whereas, starved animals did not. This finding of variable fluid homeostasis is ascribed to the different nutritional status of the animals investigated, and has considerable implications.

Animals↗
PubMed1993

The superoxide dismutase mimic TEMPOL protects cultured rabbit lens epithelial cells from hydrogen peroxide insult.

The superoxide dismutase mimic, 4-hydroxy TEMPO (TEMPOL), was used to investigate the mechanism by which H2O2 damages cultured rabbit lens epithelial cells and to identify some of the targets of H2O2 insult. Most studies aimed at determining the mechanism by which H2O2 exerts its cytotoxic effect have used iron chelators to prevent the generation of the damaging hydroxyl radical. Since TEMPOL does not chelate transition metals, we were afforded an additional means of investigating the mechanism by which H2O2 exerts its cytotoxicity. Cells at low or high density were cultured in MEM containing 5 mM TEMPOL and exposed to a single sub-lethal dose of 0.05 or 0.5 mM H2O2, respectively. Analysis of EPR spectra indicated that TEMPOL was stable in MEM, did not destroy H2O2 and penetrated the intracellular fluid. TEMPOL prevented or curtailed the H2O2-induced inhibition of cell growth, blebbing of the cell membrane, the decrease in NAD+, the activation of poly ADP-ribose polymerase, an enzyme involved in DNA repair, and limited the induction of single strand breaks in DNA normally brought about by H2O2. TEMPOL did not prevent the H2O2-induced decrease in reduced glutathione, lactate production, and the activity of glyceraldehyde 3-phosphate dehydrogenase, or the H2O2-induced increases in oxidized glutathione and hexose monophosphate shunt activity. Addition of TEMPOL 1-15 min after exposure of cells to H2O2 offered partial protection from the inhibition of cell division. TEMPOL at 5 mM did not inhibit cell growth. These results, coupled with our other findings suggest that some of the H2O2-induced damage in cultured rabbit LECs is mediated by intracellular redox-active metals involved in the Haber-Weiss cycle. Cellular changes not protected by TEMPOL, including attack of H2O2 on the thiol groups of GSH (mediated through glutathione peroxidase) and G3PDH, are likely brought about by H2O2 itself and not by reactions of oxygen free-radicals generated from H2O2.

Animals↗
PubMed1986

Dibucaine stimulation of p-aminohippurate accumulation in rat kidney cortical slices.

We studied the effects of dibucaine on p-aminohippurate (PAH) transport using rat kidney cortical slices. Addition of dibucaine in concentrations from 0.01 to 0.1 mM stimulated PAH accumulation in a concentration-dependent way; at higher concentrations, accumulation was inhibited. Kinetic studies showed that dibucaine increased the apparent maximal activity of PAH transport, whereas the apparent Km remained essentially constant. The efflux of PAH from the slices was significantly depressed by the drug. Dibucaine had no significant effect on the sodium gradient, medium to intracellular fluid. The drug had biphasic effects on hypotonic hemolysis; at lower concentrations (up to 0.2 mM) it protected erythrocytes, and at much higher concentrations, it has a lytic effect. The pattern of the membrane-stabilizing action of dibucaine was similar to that of the stimulation of PAH accumulation. These results indicate that dibucaine markedly stimulated accumulation of PAH. Stimulation by this drug of PAH transport cannot be explained by the increase in the sodium gradient; it may be due at least in part to membrane stabilization.

Aminohippuric Acids↗
PubMed1981

Cytoplasmic and membrane proteins of yersiniae cultivated under conditions simulating mammalian intracellular environment.

A procedure is described for fractionating Yersinia grown in small cultures into inner and outer membranes and soluble cytoplasmic proteins. The procedure was applied to the three recognized species of the genus grown under conditions simulating mammalian intracellular fluid with respect to Ca2+ and Mg2+. These conditions are known to elicit the production of the plague virulence antigen V. Isolates capable of making this antigen were compared with virulence-antigen-negative derivatives by two-dimensional electrophoresis. The V antigen was localized to the soluble protein fraction as a peptide that comigrates with the major component of a specific immunoprecipitate. This peptide had an apparent molecular weight of 38,000 and was not found in either apparent molecular weight of 38,000 and was not found in either membrane fraction. The comparison of virulence antigen-producers and nonproducers of Y. pseudotuberculosis and Y. enterocolitica revealed large qualitative and quantitative differences in outer membrane protein patterns, whereas the same comparison for Y. pestis showed only minor differences. The complexity of changes in the various protein fractions corroborate data in the literature indicating that extensive physiological changes occur in virulent organisms cultivated under simulated intracellular conditions.

Animals↗
PubMed1992

Altered tissue polyamine levels due to ornithine-alpha-ketoglutarate in traumatized growing rats.

All cells contain significant amounts of polyamines (PA), and their concentrations are highly regulated. Metabolic activity within a tissue may be reflected in the amount of intracellular PA. Since trauma involves accelerated death and regeneration of tissues, the related levels of PA in extracellular and intracellular fluids may reflect altered protein metabolism. Trauma induces an increased excretion of urinary PA, and the tissues responsible for this whole-body activity are not known. During posttraumatic nutritional management, supplementation with ornithine-alpha-ketoglutarate (OKG) seems to improve nitrogen economy. The present study evaluates the significance of muscle, liver, and intestine PA responses in traumatized (bilateral femur fractures) rats to the feeding of an isonitrogenous liquid diet supplemented with or without OKG. Uninjured control rats were pair-fed with respective traumatized rats. After 2 days of starvation and 4 days of feeding, the traumatized and control rats were killed and the tissues were excised and analyzed. Starvation decreases and refeeding increases urinary PA excretion. Trauma-induced PA response is predominantly seen in muscle tissues, and this may be responsible for parallel increases in PA excretion. Liver PA responses show a varying tendency confirming the increased protein synthetic activity due to trauma. Intestine has the highest intracellular PA levels, and there is a general smaller (statistically insignificant) increase in all the individual PA contents due to trauma. OKG supplementation augments tissue and urine PA responses in control rats; however, in trauma rats muscle PA levels show very little change, although nitrogen retention is significantly better (88% to 77%). Mechanistic studies are needed to evaluate the significances of the time-dependent, injury-induced, individual intracellular PA levels.

Acetylation↗
PubMed1998

Activation of a Cl--conductance by protein kinase-dependent phosphorylation in cultured rat retinal pigment epithelial cells.

While chloride conductances are involved in signals of the electroretinogram generated by the retinal pigment epithelium (RPE), patch-clamp experiments of freshly isolated or cultured RPE cells have shown that potassium conductances predominate. The purpose of this study was to investigate mechanisms which activate Cl--conductances in RPE cells. Membrane currents of cultured rat RPE cells were measured using the whole-cell configuration of the patch-clamp technique under extra- and intracellular K+-free conditions. The bath solution was hyperosmolal to the pipette solution to prevent hypoosmotic swelling. Exchange of the physiological intracellular fluid by a pipette solution with physiological levels of ATP (2 mm) induced a continuous increase of membrane conductance. Conductance was blocked by DIDS (1 mm), and showed a reversal potential close to the Nernst potential for Cl-. When the experiments were carried out under conditions in which all cations, and not only potassium, were replaced by NMDG, the same responses could be observed. Current activation was independent of extracellular calcium. Chloride currents were also induced when ATPgammaS or AMP-PNP were used instead of ATP. In the presence of AMP-PNP currents were 10 times smaller than in the presence of ATP or ATPgammaS. In cells preincubated with staurosporine or chelerythrine no currents were induced. Establishing the whole-cell configuration with ATP and with myristoylated PKC substrate in addition, no voltage-dependent currents were activated. We conclude that ATP hydrolysis leads to activation of chloride currents via PKC in the whole-cell configuration. The perforated patch configuration, with the intracellular compartment intact, no currents were induced under otherwise identical experimental conditions. Inhibition of phosphatase by calyculin (10 nm) in the perforated-patch configuration did not change membrane conductance. In the intact cell, chloride conductance is possibly inhibited by a cytosolic factor which is washed out when the whole-cell configuration is established.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed2006

Whole-body volume regulation and escape from antidiuresis.

Both individual cells and organs regulate their volume in response to sustained hypo-osmolality via solute and water losses. Similar processes occur in the whole body to regulate the volumes of extracellular fluid (ECF) and intravascular spaces toward normal levels. Body water losses occur via the phenomena "escape from antidiuresis"; solute losses occur through the secondary natriuresis induced by water retention. As a result of resistance to arginine vasopressin (AVP) signaling, escape from antidiuresis is caused by downregulation of kidney aquaporin-2 expression despite high AVP plasma levels. Recent data have implicated downregulation of vasopressin V2R as a potential mechanism of resistance, and suggest that this may be a result of decreased intrarenal angiotensin II signaling in combination with increased intrarenal nitric oxide and prostaglandin E2 signaling. The natriuresis that results in volume regulation of the ECF and vascular spaces is the result of intrarenal hemodynamic changes produced by volume expansion, but the degree to which these effects are modulated by aldosterone secretion and the activity of distal sodium cotransporters and channels remains to be elucidated. The clinical implication of these volume-regulatory processes is that the chronic hyponatremic state is one of water retention and solute losses from intracellular fluid and ECF compartments. The degree to which solute losses versus water retention contribute to hyponatremia will vary in association with many factors, including the etiology of the hyponatremia, the rapidity of development of the hyponatremia, the chronicity of the hyponatremia, the volume of daily water loading, and individual variability. Understanding these volume-regulatory processes allows a better understanding of many aspects of the conundrum of patients with "clinical euvolemia" and dilutional hyponatremia from AVP-induced water retention.

Angiotensin II↗
PubMed1996

Hematologic and body fluid changes during simulated high altitude exposure in naproxen-treated rats.

Arterial blood oxygen saturation, body fluid and hematological parameters were studied in control, naproxen (a prostaglandin synthesis inhibitor)-treated control, altitude-exposed, and naproxen-treated altitude-exposed rats after intermittent exposure of 8 h/d for 6 consecutive days to a simulated high altitude of 6,100 m (barometric pressure 349 +/- 3 mmHg). Arterial blood oxygen saturation was reduced in altitude-exposed rats, but increased significantly to near control level in naproxen-treated rats. On the other hand, 2,3-diphosphoglycerate in erythrocytes increased in altitude-exposed rats, but naproxen prevented this increase. The red blood cell count, hemoglobin concentration and hematocrit ratio were reduced significantly in drug-treated altitude-exposed rats when compared to the altitude-exposed group (without drug). Red cell mass was increased in the altitude-exposed group in comparison with control. Both red cell mass and mean corpuscular volume of altitude-exposed rats were shifted towards the control value when they were treated with naproxen. Drug-treated high altitude-exposure reduced the thiocyanate space, intracellular fluid volume and total body water content compared to drug-treated control rats. On the other hand, thiocyanate space and total body water content were increased significantly in drug-treated control rats in comparison with the control group.

Altitude↗
PubMedDate not supplied

A description of the changing body composition of the growing premature infant.

Data from studies of two similar groups of premature infants were used to describe the changing body composition (BC) of a "typical" premature infant, 3 to 4 weeks old, gaining weight from 1,200 to 2,000 g and being fed its mother's expressed breast milk at a metabolizable energy intake of 93.6 kcal/kg/day. Serial measurements had been made of total body water (TBW), the extracellular fluid space (ECF), nitrogen balance, and gross energy balance in one group of premature (n = 17) infants and of total body potassium (TBK) in another group (n = 23); all infants studied weighed between 900 and 2,300 g. Equations relating TBW, ECF, and TBK to body weight were derived for estimating the content of these substances at body weights between 1,200 and 2,000 g. Protein content at 1,200 g body weight was estimated from measured TBK and N:K ratio (determined from the reference fetus) at this weight. Subsequent protein content was determined from average N accretion, determined from data of N balance, and carbohydrate and ash content were estimated from reference data. The remainder of the body weight was assumed to be fat. At 1,200 g, the proposed BC of the premature infant is 72.1% water, 10.7% protein, 14.9% fat, 1.9% ash, and 0.4% carbohydrate. At 2,000 g comparable figures are 67.8% water, 11.6% protein, 18.2% fat, 1.9% ash, and 0.5% carbohydrate. The description also provides estimates of the body cell mass (BCM) and intracellular fluid (ICF), the relationship of K to the BCM and ICF, and the energy balance of the growing premature infant.

Body Composition↗
PubMed1983

Plasma prolactin levels and body fluid deficits in the rat: causal interactions and control of water intake.

A study was made of the responses of chronically hyperprolactinaemic rats to selected dipsogenic stimuli. Measurements were also made of the correlation between the state of hydration of the animal and the plasma prolactin levels. After 24 h water deprivation. S.C. isoprenaline (10 micrograms/kg body wt.) or I.P. injection (5 ml/kg body wt.) of a hypertonic solution (50% w/w) of polyethylene glycol (mol. wt 20000) there was no difference between the hyperprolactinaemic and control rats with respect to the total water intake, the time course of drinking or the urine output. After I.V. injection of 2 M-NaCl (5 ml/kg body wt.) there was no difference between the hyperprolactinaemic and control rats with respect to the total water intake or urine output. However, the hyperprolactinaemic rats drank more slowly than the controls. When angiotensin II was infused I.V. at a rate of 0.2 micrograms/min, the water intake was greater and the threshold to drinking lower in the hyperprolactinaemic than control rats. After 24 h water deprivation, plasma prolactin levels rose significantly in both the control and hyperprolactinaemic rats. When the rats were injected I.V. with hypertonic saline (5 ml, 2 M-NaCl/kg body wt.) and denied access to water, plasma prolactin levels had not changed 1 h later in either the control or hyperprolactinaemic animals. It is concluded that there is no interaction either between the plasma osmolality and prolactin secretion or between the plasma prolactin levels and the amount of water drunk in response to intracellular fluid deficits. However, prolactin secretion is stimulated by the combined intra- and extracellular deficits resulting from water deprivation and there is a clearly demonstrated interaction between prolactin and the extracellularly mediated stimulus of angiotensin II.

Angiotensin II↗