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PubMed1998

Secreted and intracellular phospholipases A2 inhibition by 1-decyl 2-octyl-glycerophosphocholine in rat peritoneal macrophages.

Compounds able to inhibit phospholipases A2 can be considered as potential anti-inflammatory drugs. In this respect, the inhibitory effect of the phospholipid analogue 1-decyl 2-octyl-rac-glycero-3-phosphocholine (decyloctyl-GPC) added to the culture medium of rat peritoneal macrophages stimulated with ionophore A23187 was determined. (a) The substrate of phospholipase A2 1-octadecanoyl 2-[14C]eicosatetraenoyl-sn-glycero-3-phosphocholine ([14C]20:4-GPC) was added to the culture medium. In macrophages + extracellular fluids, its hydrolysis at the 2-position, produced [14C]non-phosphorous lipids which reached 12% of the dose at 0.14 microM, 73% at 0.9 and > 90% at 1.6 microM; in experiments where macrophages and extracellular fluids were analyzed separately, decyloctyl-GPC initially added at 4 microM, significantly inhibited the release of [14C]fatty acids and the eicosanoid synthesis, demonstrating its ability to inhibit secreted and/or intracellular phospholipases A2. (b) Extracellular fluids were separated from the macrophages and incubated with [14C]20:4-GPC: 48% of the dose was hydrolyzed by extracellular fluid-associated secreted phospholipase A2 and decyloctyl-GPC at 3 microM, reduced this hydrolysis by 50%. (c) [3H]arachidonic acid ([3H]20:4) was added to the culture medium and was esterified in the macrophage membrane phospholipids. Activation of intracellular phospholipase A2 induced the release of [3H] fatty acids and eicosanoid synthesis. These releases were inhibited by 50% with decyloctyl-GPC added at 4 microM. (d) [3H]20:4 and [14C]20:4-GPC were added to the culture medium of the macrophages. [3H] and [14C] fatty acids and eicosanoids were released in macrophages or extracellular fluids. They were significantly reduced by the phospholipid analogue added at 4 microM. It is concluded that secreted and intracellular phospholipases A2 were both inhibited by decyloctyl-GPC which extensively reduced the 20:4 release from exogenous and membrane phospholipids and therefore eicosanoid synthesis.

Animals↗

PubMed2004

Effect of mild hypothermia on brain dialysate lactate after fluid percussion brain injury in rodents.

OBJECTIVE: To investigate the effects of mild hypothermia on brain microdialysate lactate after fluid percussion traumatic brain injury (TBI) in rats. METHODS: Brain dialysate lactate before and after fluid percussion brain injury (2.1 +/- 0.2 atm) was measured in rats with preinjury mild hypothermia (32 degrees C), postinjury mild hypothermia (32 degrees C), injury normothermia (37 degrees C), and the sham control group. Mild hypothermia (32 degrees C) was induced by partial immersion in a water bath (0 degrees C) under general anesthesia and maintained for 2 hours. RESULTS: In the normothermia TBI group, brain extracellular fluid lactate increased from 0.311 +/- 0.03 to 1.275 +/- 0.08 mmol/L within 30 minutes after TBI (P < 0.01) and remained at a high level (0.546 +/- 0.05 mmol/L) (P < 0.01) at 2 hours after injury. In the postinjury mild hypothermic group, brain extracellular fluid lactate increased from 0.303 +/- 0.03 to 0.875 +/- 0.05 mmol/L at 15 minutes after TBI (P < 0.01) and then gradually decreased to 0.316 +/- 0.04 mmol/L at 2 hours after TBI (P > 0.05). In the preinjury mild hypothermic group, brain extracellular fluid lactate remained at normal levels after injury (P > 0.05). CONCLUSION: The cerebral extracellular fluid lactate level increases significantly after fluid percussion brain injury. Preinjury mild hypothermia completely inhibits the cerebral lactate accumulation, and early postinjury mild hypothermia significantly blunts the increase of cerebral lactate level after fluid percussion injury.

Animals↗

PubMed1975

Restitution of blood volume after hemorrhage: mathematical description.

An analytical model was developed to simulate the restitution of blood volume after hemorrhage. This model was used to test two previously proposed hypotheses for the restoration of plasma oncotic pressure required for full restitution of blood volume: increased lymphatic flow or decreased trans-capillary leakage of albumin. Neither hypothesis could account for the temporal and quantitative features of experimentally observed restitution of blood volume. An alternate hypothesis, that restitution of blood volume results from a fluid shift from intracellular-extracellular fluid shift occurs in dogs treated with high doses of cortisol analog. Thus the results of the simulation support the hypothesis that full restitution of blood volume requires an intracellular-extracellular fluid shift. This fluid shift may be mediated by high circulating levels of cortisol secondary to hemorrhage.

Animals↗

PubMed1981

Body fluid volumes in the spontaneously hypertensive rat.

1. Plasma volume, packed cell volume (PCV), blood pressure, extracellular fluid volume (ECFV) and evans blue disappearance rate were measured in conscious spontaneously hypertensive rats and in weight-matched Wistar normotensive rats. 2. Over the weight range studied (250-350 g), plasma and blood volumes were significantly lower in the spontaneously hypertensive rat. Extracellular fluid volumes were similar in the two groups. PCV and Evans blue disappearance rates were significantly higher in the spontaneously hypertensive rat. 3. Negative correlations were obtained between plasma volume and mean arterial pressure and between the plasma/interstitial fluid volume ratio and mean arterial pressure. 4. The normal extracellular fluid volume and the lack of correlation with mean arterial pressure excludes volume expansion as a pressor mechanism during the established phase of hypertension in the spontaneously hypertensive rat.

Animals↗

PubMed1993

The influence of Ringer's lactate and gelatin infusion on the internal fluid balance of healthy volunteers measured by a non-invasive conductivity technique.

Eight healthy male volunteers received in random order at an interval of 1 week 2 litres of Ringer's lactate or 0.8 litre of gelatin (Gelofusine) over half an hour, after overnight fasting. At the end of the infusion period, blood volume and mean arterial pressure had increased significantly in both groups but the increase in blood volume was more pronounced with the colloid. Extracellular fluid volume increased significantly after Ringer's lactate, while a significant decrease was noticed after gelatin. A small decrease in intracellular fluid volume was noted after infusion of Gelofusine, whereas it did not change after infusion of Ringer's lactate. During the 30 min after infusion, blood volume decreased significantly after both treatments but after the colloid it remained higher than the initial value. During the post-infusion period, no significant changes in either intra- or extracellular volume were seen after either treatments. At the end of the study, urine production was significantly more after the Ringer's lactate. It can be concluded that infusion of 0.8 litre of gelatin results in a larger and longer lasting increase in blood volume than 2 litres of Ringer's lactate, probably due to mobilization of extracellular fluid volume. It also leads to extracellular fluid accumulation. The decrease in blood volume after infusion is caused by increased urine production, since no changes were seen in intra- and extracellular fluid volume during this period.

Adult↗

PubMed1999

Low-dose whole-body irradiation induces alteration of protein expression in mouse splenocytes.

In previous studies, the stimulatory effect on immunological function and adaptive response in splenocytes were found after exposure of mice to low-dose whole-body irradiation (LD-WBI). Protein synthesis was found to be required for these responses. The present study, therefore, attempts to investigate the protein changes in mouse splenocytes after exposure to LD-WBI. Two-dimensional gel electrophoresis was used to show the alterations of proteins in nuclei, cytoplasm and extracellular fluid of the splenocytes at 4 h after mice exposed to 75 mGy X-rays. As compared to control, changed expressions of 20, 15 and 6 proteins, in sizes ranging from 10 to 69 kDa with pI of 5.0-8.2, were found in the nuclei, cytoplasm and extracellular fluid of splenocytes, respectively. One protein, shown in the cytoplasm of splenocytes of control mice, appeared in extracellular fluid of splenocytes after LD-WBI. Two proteins, shown in cytoplasm, and one protein, shown in extracellular fluid of splenocytes in control mice, appeared in the nuclei after LD-WBI. Time-course of protein synthesis varied in different proteins after LD-WBI. These results suggest that alterations of protein expressions and redistribution of proteins between intracellular and extracellular compartments occurred in the splenocytes after LD-WBI. Protein extract from LD-WBI splenocytes was fractionated by Sephadex G-100. Fractions 61-80 contained proteins able to protect lymphocytes in vitro from radiation-induced chromosome aberrations. These findings are of importance in elucidating mechanisms of immuno-enhancement and adaptive response induced by low-dose radiation. although the features and the functions of these proteins remain to be elucidated in future studies.

Animals↗

PubMed1985

Effect of extracellular water volume on the distribution kinetics of beta-lactam antibiotics as a function of age.

The distribution kinetics of cefazolin in rats has been examined at four different ages (1, 7, 50 and 100 weeks). The steady state distribution volume of cefazolin, estimated from the plasma time course after i.v. injection of 20 mg/kg, varied between 136 ml/kg (50-week-old rats) and 297 ml/kg (1-week-old rats). The extracellular fluid volume, obtained from the steady state distribution volume of inulin, varied between 126 ml/kg (50-week-old rats) and 370 ml/kg (1-week-old rats). There was a good correlation between the steady state distribution volume of cefazolin and extracellular fluid volume (r = 0.977). The influence of changes on the value of the plasma unbound fraction and extracellular fluid volume on the tissue-to-plasma partition coefficient of beta-lactam antibiotics was simulated by using a physiological pharmacokinetic model. The results of the simulation showed that extracellular fluid volume is an important factor affecting the distribution volume of beta-lactam antibiotics and that plasma binding plays a minor role on it. The experimental and simulation results suggested that the change in the interstitial fluid volume is a determinant factor in the age-related changes in the distribution volume of beta-lactam antibiotics.

Aging↗

PubMed2003

Role of nitric oxide in ethanol-induced ascorbic acid release in striatum of freely moving mice.

In the present study, in vivo brain microdialysis coupled with high performance liquid chromatography (HPLC) and electrochemical detection were used to evaluate the effects of either L-arginine (L-Arg), the substrate of nitric oxide synthase (NOS), Nomega-nitro-L-arginine methyl ester hydrochloride (L-NAME), a non-selective NOS inhibitor, or sodium nitroprusside (SNP), a donor of NO, on the ethanol-induced release of ascorbic acid (AA) in the striatum of freely moving mice. Drugs were administered intrastriatally via the microdialysis probe and ethanol (2-4 g/kg) was administered intraperitoneally. The results showed that L-arginine (1-10 mg/ml) had no effect on either the basal AA contents in striatal extracellular fluid or the ethanol-induced release of AA. L-NAME (10(-4) to 10(-3) mg/ml) and SNP (10(-4) to 10(-3) mg/ml) both reduced the basal AA concentrations in striatal extracellular fluid. L-NAME significantly inhibited ethanol-induced release of AA, while SNP only had a transient inhibitory effect on the ethanol-induced release of AA. SNP significantly increased dehydroascorbic acid (DHAA) contents and DHAA/AA ratio but had no effect on the total AA contents (AA and DHAA contents) in striatal extracellular fluid, while L-NAME had no effect on DHAA contents but decreased the total AA contents in striatal extracellular fluid. Only high concentration L-NAME induced a transient increase in DHAA/AA ratio. Our results suggest that nitric oxide (NO) might not directly be involved in the mechanism of ethanol-induced release of AA in mouse striatum.

Animals↗

PubMed1999

Extracellular glucose concentrations in the rat hippocampus measured by zero-net-flux: effects of microdialysis flow rate, strain, and age.

The concentration of glucose in the brain's extracellular fluid remains controversial, with recent estimates and measurements ranging from 0.35 to 3.3 mM. In the present experiments, we used the method of zeronet-flux microdialysis to determine glucose concentration in the hippocampal extracellular fluid of awake, freely moving rats. In addition, the point of zero-net-flux was measured across variations in flow rate to confirm that the results for glucose measurement were robust to such variations. In 3-month-old male Sprague-Dawley rats, the concentration of glucose in the hippocampal extracellular fluid was found to be 1.00 +/- 0.05 mM, which did not vary with changes in flow rate. Three-month-old and 24-month-old Fischer-344 rats both showed a significantly higher hippocampal extracellular fluid glucose concentration, at 1.24 +/- 0.07 and 1.21 +/- 0.04 mM, respectively; there was no significant difference between the two age groups. The present data demonstrate variation in extracellular brain glucose concentration between rat strains. When taken together with previous data showing a striatal extracellular glucose concentration on the order of 0.5 mM, the data also demonstrate variation in extracellular glucose between brain regions. Traditional models of brain glucose transport and distribution, in which extracellular concentration is assumed to be constant, may require revision.

Aging↗

PubMed1974

Flux of free fatty acids among host tissues, ascites fluid, and Ehrlich ascites carcinoma cells.

The role of plasma free fatty acids (FFA) in the transport of fatty acids from host tissues to Ehrlich ascites carcinoma in mice was studied. [9,10-(3)H] Palmitate complexed to mouse serum (albumin) was injected either intraperitoneally or intravenously into unanesthetized tumor-bearing mice. The incorporation of radioactivity into tumor extracellular fluid FFA, tumor cell FFA, neutral lipid, phospholipid, water-soluble material in cells and fluid, plasma FFA, host carcass total lipid fatty acids, and water-soluble (i.e., nonlipid) material was measured. In addition, the quantity of fatty acid in each of the above lipid fractions was determined. The data were analyzed by multicompartmental analysis (SAAM) using a digital computer, and fractional rate constants of FA movement within and out of the host-tumor system were calculated. These rate constants and pool size measurements were used to estimate the corresponding fluxes. Although FFA in the tumor's extracellular fluid were replaced rapidly, almost none of the newly formed fluid FFA was derived from plasma FFA. Moreover, the transfer of FFA from the tumor extracellular fluid FFA to plasma FFA was virtually negligible. We suggest that the net amount of FFA required to replace the fluid FFA utilized for tumor energy and growth may be derived from direct transfer of FFA from host tissues to the ascitic fluid and that plasma FFA is not an intermediate in this transport process. The transport of FFA from the host to tumor cell lipids through the tumor extracellular fluid was about 26-fold greater than that required to account for net lipid accumulation during growth.

Animals↗

PubMed1985

Low density lipoprotein degradation by rat mast cells. Demonstration of extracellular proteolysis caused by mast cell granules.

The interaction between rat serosal mast cells and low density lipoproteins (LDL) was studied in vitro. When rat 125I-LDL was incubated with mast cells, it was bound to a binding site on the mast cell surface but was not internalized by the cells. Even though 125I-LDL was not internalized, its protein component, apolipoprotein B, was rapidly degraded. The proteolytic activity responsible for the degradation of apolipoprotein B was present in the extracellular fluid of mast cells. It could be shown that the degradation was caused entirely by specific cell organelles of mast cells, the granules, which were spontaneously released into the extracellular fluid during preparation and incubation of the cells. In contrast to uncontrolled spontaneous degranulation, a controlled specific degranulation of mast cells can be induced by treating the cells with the compound 48/80. When increasing amounts of 48/80 were added to mast cell suspensions, a dose-dependent release of granules was observed and an increase in the rate of 125I-LDL degradation resulted. The increase in 125I-LDL degradation closely followed the increase in granule release. Thus, a quantitative relationship between the amount of granules present in the extracellular fluid and the amount of degradation of 125I-LDL could be established. The apolipoprotein part of LDL was extensively degraded by isolated mast cell granules. Analysis by polyacrylamide gel electrophoresis showed that upon incubation of LDL with isolated granules, the apolipoprotein B band rapidly disappeared with simultaneous appearance of several low molecular weight bands. The degradation of 125I-LDL by mast cell granules proceeded optimally at neutral pH and at physiological ionic strength. The results show that mast cell granules are able to efficiently degrade LDL in vitro, once released from mast cells into the extracellular fluid.

Animals↗

PubMed2006

Purification and characterization of an alkaline lipase from Pseudomonas aeruginosa isolated from putrid mineral cutting oil as component of metalworking fluid.

Extracellular lipase was isolated and purified from the culture broth of Pseudomonas aeruginosa, an extremophile which naturally grows in water-soluble mineral cutting oil (pH 10) used as metalworking fluid (MWF) for cooling and lubrication in industrial metalworking processes. The molecular mass of the purified lipase was estimated by SDS-PAGE to be 54 kDa. The optimum pH and temperature were 11 and 70 degrees C, respectively. The enzyme is stabile over a broad pH range (pH 4-11.5). The lipase preferably acted on triacylglycerols with medium-chain fatty acids. The lipase was inhibited strongly by Zn(2+), Hg(2+), Cu(2+) and slightly by Ca(2+) and Mg(2+). Non-ionic detergents and sodiumdeoxycholate enhanced lipase activity. Alkaline lipase from P. aeruginosa, capable of growing in a water-restricted medium has excellent properties and good potential for biotechnological applications in the metal industry. Its marked stability and activity in organic solvents suggest that this lipase is highly suitable as a biotechnological tool in a water-restricted medium with a variety of applications including organosynthetic reactions and the control and prevention of MWF putrification in the metal industry.

Biotechnology↗

PubMed2004

Hormones: what the testis really sees.

Various barriers in the testis may prevent hormones from readily reaching the cells they are supposed to stimulate, especially the hydrophilic hormones from the pituitary. For example, LH must pass through or between the endothelial cells lining the blood vessels to reach the surface of the Leydig cells, and FSH has the additional barrier of the peritubular myoid cells before it reaches the Sertoli cells. The specialised junctions between pairs of Sertoli cells would severely restrict the passage of peptides from blood to the luminal fluid and therefore to the cells inside this barrier, such as the later spermatocytes and spermatids. There is evidence in the literature that radioactively labelled LH does not pass readily into the testis from the blood, and the concentration of native LH in the interstitial extracellular fluid surrounding the Leydig cells in rats is only about one-fifth of that in blood plasma. Furthermore, after injection with LHRH, there are large rises in LH in the blood within 15 min, at which time the Leydig cells have already responded by increasing their content of testosterone, but with no significant change in the concentration of LH in the interstitial extracellular fluid. Either the Leydig cells respond to very small changes in LH, or the testicular endothelial cells in some way mediate the response of the Leydig cells to LH, for which there is now some evidence from co-cultures of endothelial and Leydig cells. The lipophilic steroid hormones, such as testosterone, which are produced by the Leydig cells, have actions within the seminiferous tubules in the testis but also in other parts of the body. They should pass more readily through cells than the hydrophilic peptides; however, the concentration of testosterone in the fluid inside the seminiferous tubules is less than in the interstitial extracellular fluid in the testis, especially after stimulation by LH released after injection of LHRH and despite the presence inside the tubules of high concentrations of an androgen-binding protein. The concentration of testosterone in testicular venous blood does not rise to the same extent as that in the interstitial extracellular fluid, suggesting that there may also be some restriction to movement of the steroid across the endothelium. There is a very poor correlation between the concentrations of testosterone in fluids from the various compartments of the testis and in peripheral blood plasma. Determination of the testosterone concentration in the whole testis is also probably of little predictive value, because the high concentrations of lipid in the Leydig cells would tend to concentrate testosterone there, and hormones inside these cells are unlikely to have any direct effect on other cells in the testis. The best predictor of testosterone concentrations around cells in the testis is the level of testosterone in testicular venous blood, the collection of which for testosterone analysis is a reasonably simple procedure in experimental animals and should be substituted for tissue sampling. There seems to be no simple way of determining the concentrations of peptide hormones in the vicinity of the testicular cells.

Animals↗

PubMed1983

Neural mechanisms of volume regulation.

Under steady-state conditions, urinary sodium excretion matches dietary sodium intake. Because extracellular fluid osmolality is tightly regulated, the quantity of sodium in the extracellular fluid determines the volume of this compartment. The left atrial volume receptor mechanism is an example of a neural mechanism of volume regulation. The left atrial mechanoreceptor, which functions as a sensor in the low-pressure vascular system, has a well-defined compliance relating intravascular volume to filling pressure and responds to changes in wall tension by discharging into afferent vagal fibers. These fibers have appropriate central nervous system representation whose related efferent neurohumoral mechanisms regulate thirst, renal excretion of water and sodium, and the redistribution of the extracellular fluid volume.

Animals↗

PubMed1976

[Renal water-electrolyte excretion and its control mechanisms. Current status of knowledge].

The literature on hydronatriuresis control processes operating at the level of individual renal functional units and of the organ as a whole is analysed. 1) Elementary sodium salt and water tubular transport mechanisms. In converting the filtrate into urine, the kidney expends metabolic energy: this is used in the (active) transport of sodium salts; (passive) transport of water takes place along the osmotic gradients created by salt transfer. The proximal tubules reabsorb the sodium bic-rbonate actively. The reabsorption of the osmitic equivalent of water has the effect of concentrating NaCl in the tubular fluid. An important role in the reabsorption of NaCl is played by passive diffusion from the lumen to the interstitial fluid; the remainder is transferred actively, perhaps by an electrically neutral pump. With respect to the other nephronic segments, the proximal tubule has a relatively high passive permeability to water and salts: active transport here must not surmount high friction resistances nor take place against important concentration gradients. The low permeability of the distal nephron, on the other hand, increases the energy cost of salt transport; for the same reason, important electrochemical gradients are created and the composition of tubular fluid is drastically altered. 2) Elementary mechanisms of tubular potassium transport. Potassium is reabsorbed actively along the whole nephron by a luminal pump. The proximal tubules and Henle loops promote practically complete absorption of filtrated potassium. The distal tubules and collectors have the two-fold capacity of secreting and reabsorbing cation: the quantity of potassium excreted with the urine depends on the degree of excess of the secretion process. At distal tubular level, potassium secretion is a passive phenomenon dependent on the favourable transluminal gradient of the cation's electrochemical potential. 3) Renal function and volume homoeostasis of extracellular fluid. The organism's sodium content is largely controlled by renal excretion of sodium; homoeostasis of the sodium mass guarantees volume homoeostasis of the extracellular fluid through thirst and osmotic secretion of ADH. Extracellular fluid volume errors are picked up by the organism to the extent to which they translate themselves into pressure variations in the low pressure vascular system or into variations in haematic constituent concentration within the vascular sector, produced with velocities independent, at least in the short term, of the volume of extracellular fluid. In control of natriuria are the glomerular filtrate, intrarenal distribution of blood flow and tubular reabsorption of sodium; in its turn, the latter is subject to nervous and hormonal influences and influences from the physical environment surrounding the nephrons...

Aldosterone↗

PubMedDate not supplied

Extravascular lung water and peripheral volume status in hemodialysis patients with and without a history of heart failure.

Determining volume status in hemodialysis patients with a history of congestive heart failure (CHF) is difficult. Extravascular lung water (EVLW) may be derived from blood ultrasound velocity changes following injections of 0.9% and 5% saline. Bioimpedance spectroscopy can measure total body water (TBW) and its intracellular fluid (ICF) and extracellular fluid (ECF) compartments. We studied 29 clinically euvolemic hemodialysis patients, 12 of whom had a history of CHF. The ECF and ICF were measured before dialysis, and EVLW was measured during dialysis. Values of EVLW were similar between patients without CHF and those with CHF (3.55 ml/kg +/- 0.94 SD versus 3.88 ml/kg +/- 0.82 SD, respectively; p = NS). The ECF/ICF ratio was higher among patients with a history of CHF (1.27 +/- 0.29) than among those without such a history (1.04 +/- 0.04; p < 0.05), indicating that ECF volume overload was present in both groups, but was higher in those with a CHF history. There was a positive correlation between EVLW and ECF/ICF ratios (r = 0.54, p < 0.01). Measurements of EVLW were higher in two pulmonary edema patients ((7.95 ml/kg and 5.95 ml/kg; p < 0.05). The results of this study suggest that 1) hemodialysis patients with a history of CHF have more ECF volume overloaded than those without such a history; 2) the degree of ECF expansion is associated with increasing EVLW volume, even in patients without pulmonary edema; and 3) ECF volume expansion eventually exceeds limits and pulmonary edema occurs. These developing technologies of volume measurement may be of value in this challenging clinical area.

Aged↗

PubMed2002

Effect of mineralocorticoid deficiency on ion and urea transporters and aquaporin water channels in the rat.

Mineralocorticoid deficiency is associated with impaired urinary concentration and dilution. The present investigation was undertaken to determine the effects of selective mineralocorticoid deficiency on renal sodium and urea transporters and aquaporin water channels and whether these perturbations can be reversed by maintenance of extracellular fluid volume. Mineralocorticoid deficiency was induced by bilateral adrenalectomies with glucocorticoid replacement. Mineralocorticoid deficient rats receiving plain drinking water (MDW) were compared with mineralocorticoid deficient rats receiving saline-drinking water (MDS) in order to maintain extracellular fluid volume, and with controls (CTL). In MDW rats, there was a significant decrease in renal outer medulla Na-K-2Cl co-transporter and outer medulla Na-K-ATPase as well as an increase in inner medulla aquaporins 2 and 3. There were no significant changes in aquaporin-1, aquaporin-4, or urea transporters. These alterations were reversed with maintenance of extracellular fluid volume in MDS rats. Our findings indicate that mineralocorticoid deficiency in the rat is associated with alterations in factors involved in the countercurrent concentrating mechanism (Na-K-2Cl, Na-K-ATPase) and osmotic water equilibration in the collecting duct (AQP2, AQP3). Maintenance of sodium balance and extracellular fluid volume is associated with normalization of these perturbations.

Adrenalectomy↗

PubMed1989

Vasopressin and water distribution in rats with DOCA-salt hypertension.

The role of vasopressin in the regulation of body water volume and its distribution to intravascular, interstitial and intracellular compartments, and the importance of particular body water compartments in the pathogenesis of DOCA-salt hypertension were studied in young Brattleboro rats. Vasopressin-deficient, vasopressin-synthesizing and vasopressin-deficient rats chronically supplemented with deamino-8-D-arginine vasopressin (dDAVP) were compared with water-drinking controls. The chronic DOCA-salt treatment caused a marked hypertension in vasopressin-synthesizing animals; in these animals body water was slightly increased due to the expansion of extra-cellular fluid volume whereas intracellular water tended to decrease, so that the ratio of extracellular fluid volume to intracellular water rose significantly. The development of DOCA-salt hypertension was attenuated in the vasopressin-deficient rats, which had a similar level of total body water, slightly increased intracellular water and significantly decreased extracellular fluid volume compared with the hypertensive vasopressin-synthesizing rats. Consequently, in the vasopressin-deficient rats, the ratio of extracellular fluid volume to intracellular water did not differ from that of controls. A vasopressin deficiency was associated with a failure to expand the interstitial fluid volume although plasma volume was increased. Unaltered total body water together with elevated plasma osmolality indicated an extracellular water deficiency in DOCA-salt-treated vasopressin-deficient rats. Chronic dDAVP supplementation restored the body fluid pattern and the hypertensive response of the DOCA-salt-treated vasopressin-deficient rats. In conclusion, the antidiuretic effects of vasopressin are necessary for the interstitial fluid volume expansion that is essential for a full development of DOCA-salt hypertension.

Animals↗