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PubMed2005

Transcriptional analysis of a gene cluster involved in glucose tolerance in Zymomonas mobilis: evidence for an osmoregulated promoter.

Exponentially growing cells of Zymomonas mobilis normally exhibit a lag period of up to 3 h when they are transferred from a liquid medium containing 2% glucose to a liquid medium containing 10% glucose. A mutant of Z. mobilis (CU1) exhibited a lag period of more than 20 h when it was grown under the same conditions, whereas it failed to grow on a solid medium containing 10% glucose. The glucose-defective phenotype of mutant CU1 was due to a spontaneous insertion in a putative gene (ORF4) identified as part of an operon (glc) which includes three additional putative genes (ORF1, ORF2, and ORF3) with no obvious involvement in the glucose tolerance mechanism. The common promoter controlling glc operon transcription, designated P(glc), was found to be osmoregulated and stimulated by the putative product of ORF4 in an autoregulated fashion, as indicated by expression of the gfp reporter gene. Additionally, reverse transcriptase PCR analysis showed that the gene cluster produces a single mRNA, which verified the operon organization of this transcription unit. Further transcriptional analysis demonstrated that glc operon expression is regulated by the concentration of glucose, which supported the hypothesis that this operon is directly involved in the uncharacterized glucose tolerance mechanism of Z. mobilis.

Amino Acid Sequence↗
PubMed2007

Substantia nigra osmoregulation: taurine and ATP involvement.

An extracellular nonsynaptic taurine pool of glial origin was recently reported in the substantia nigra (SN). There is previous evidence showing taurine as an inhibitory neurotransmitter in the SN, but the physiological role of this nonsynaptic pool of taurine has not been explored. By using microdialysis methods, we studied the action of local osmolarity on the nonsynaptic taurine pool in the SN of the rat. Hypoosmolar pulses (285-80 mosM) administered in the SN by the microdialysis probe increased extrasynaptic taurine in a dose-dependent way, a response that was counteracted by compensating osmolarity with choline. The opposite effect (taurine decrease) was observed when osmolarity was increased. Under basal conditions, the blockade of either the AMPA-kainate glutamate receptors with 6-cyano-7-nitroquinoxaline-2,3-dionine disodium or the purinergic receptors with pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid modified the taurine concentration, suggesting that both receptors modulate the extrasynaptic pool of taurine. In addition, these drugs decreased the taurine response to hypoosmolar pulses, suggesting roles for glutamatergic and purinergic receptors in the taurine response to osmolarity. The participation of purinergic receptors was also supported by the fact that ATP (which, under basal conditions, increased the extrasynaptic taurine in a dose-dependent way) administered in doses saturating purinergic receptors also decreased the taurine response to hypoosmolarity. Taken together, present data suggest osmoregulation as a role of the nonsynaptic taurine pool of the SN, a function that also involves glutamate and ATP and that could influence the nigral cell vulnerability in Parkinson's disease.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1983

Osmoregulation of thirst and vasopressin secretion in human subjects: effect of various solutes.

Various hypertonic solutions were infused in healthy human volunteers to determine their effect on thirst and vasopressin secretion. Hypertonic saline and mannitol produced prompt and parallel increases in plasma osmolality and vasopressin concentration. For both of these solutes, there was a high degree of correlation between these measurements. The slope describing this relationship varied considerably between individuals, but the same subjects showed similar slopes with either saline or mannitol. Both solutions stimulated thirst. Hypertonic urea infusions produced a comparable rise in osmolality but produced a smaller increase in plasma vasopressin and stimulated thirst in only one of the subjects. With urea, the correlation between plasma osmolality and vasopressin was significantly lower. Within individuals, the slope describing this relationship was significantly correlated with that seen during hypertonic saline. Hypertonic glucose significantly increased plasma osmolality but decreased plasma vasopressin and had no detectable effect on thirst. We conclude that osmoregulation of vasopressin in humans is mediated by a selective osmoreceptor that is located primarily outside of the blood-brain barrier and that individual differences in osmoregulatory sensitivity are not solute specific.

Adult↗
PubMed1990

Osmoregulation of vasopressin in diabetic ketoacidosis.

Osmoregulation of arginine vasopressin (AVP) is altered in diabetic ketoacidosis (DKA). With hyperglycemia, the AVP-plasma sodium (PNa) curve is displaced to the left, whereas the AVP-osmolality (Posm) curve is displaced to the right. The shift in the Na curve is explained by either resetting of the Na set point or by glucose acting as a nonpermeable solute, substituting for Na. Conversely, putative unmeasured solutes that, like urea, fail to affect AVP have been postulated to account for the right shift in the AVP-Posm curve. Therefore the respective roles of Posm = sigma [Xi] and plasma tonicity (Pton = sigma [sigmaiXi]), i.e., the sum of concentrations of all solutes [Xi] corrected (Pton) or not (Posm) for their relative cell permeability (sigma i), were studied in DKA. Indeed, Posm = sigma [Xi] exceeds Pton = sigma [sigma iXi] in DKA, since sigma i less than 1 for glucose. Potential determinants of AVP release (Posm, Pton, and PNa) were monitored in 7 patients with DKA. Conventional correlation analysis and two-dimensional (2D) graphs reproduced the paradox of an opposite shift in PNa and Posm set points for AVP release. However, by using the concept of tonicity instead of osmolality, 3D plots instead of 2D graphs, and multiple regressions instead of correlations, the AVP-PNa and AVP-Pton curves did not appear displaced. The concept of tonicity resolved the paradox of both osmolality and Na thresholds reset in opposite directions. Indeed, in states where a solute like glucose (with sigma less than 1) contributes substantially to plasma osmolality, Posm measured in vitro by the osmometer greatly exceeds Pton perceived in vivo by the osmoreceptor.

Adolescent↗
PubMed2006

Ouabain-sensitive bicarbonate secretion and acid absorption by the marine teleost fish intestine play a role in osmoregulation.

The gulf toadfish (Opsanus beta) intestine secretes base mainly in the form of HCO3- via apical anion exchange to serve Cl- and water absorption for osmoregulatory purposes. Luminal HCO3- secretion rates measured by pH-stat techniques in Ussing chambers rely on oxidative energy metabolism and are highly temperature sensitive. At 25 degrees C under in vivo-like conditions, secretion rates averaged 0.45 micromol x cm(-2) x h(-1), of which 0.25 micromol x cm(-2) x h(-1) can be accounted for by hydration of endogenous CO2 partly catalyzed by carbonic anhydrase. Complete polarity of secretion of HCO3- and H+ arising from the CO2 hydration reaction is evident from equal rates of luminal HCO3- secretion via anion exchange and basolateral H+ extrusion. When basolateral H+ extrusion is partly inhibited by reduction of serosal pH, luminal HCO3- secretion is reduced. Basolateral H+ secretion occurs in exchange for Na+ via an ethylisopropylamiloride-insensitive mechanism and is ultimately fueled by the activity of the basolateral Na+-K+-ATPase. Fluid absorption by the toadfish intestine to oppose diffusive water loss to the concentrated marine environment is accompanied by a substantial basolateral H+ extrusion, intimately linking osmoregulation and acid-base balance.

Acids↗
PubMed1985

Osmoregulation and vasopressin secretion during pregnancy in Brattleboro rats.

Osmoregulation during pregnancy was compared in Brattleboro rats completely lacking vasopressin [homozygous (DI)], those with partial deficiency [heterozygous (HZ)], and control Long-Evans (LE) animals. Plasma osmolality (Posmol) was decreased 10-16 mosmol/kg near term in each group, whereas urine osmolality (Uosmol) was similar to that of virgin controls. This was accompanied by significant increments in water turnover similar in HZ and LE and massive in the gravid DI. Chronic vasopressin treatment increased Uosmol less in pregnant DI compared with virgins (P less than 0.001), and urinary prostaglandin E2 was increased in all gravid groups. Captopril per os failed to implicate the renin-angiotensin system in the altered water ingestive behavior of pregnancy. Basal arginine vasopressin pressure (PAVP) was similar in gravid and virgin HZ and LE, whereas the osmotic threshold for AVP secretion was lower in both pregnant groups. Increasing Posmol by dehydration or hypertonic saline led to similar increments in plasma AVP (PAVP) in pregnant and nongravid rats of each group, but sensitivity of the system delta P AVP/delta P osmol was significantly lower in HZ, a difference compatible with the decreased pituitary AVP content in the HZ strain. Data are consistent with decreases in the osmotic thresholds for AVP release (in HZ and LE) and thirst (in DI) and a need for increased AVP secretion during pregnancy.

Animals↗
PubMed1988

Osmoregulation in pseudopregnant and prolactin-treated rats: comparison with normal gestation.

Osmoregulation was studied throughout rodent pregnancy focusing on the importance of the fetoplacental unit and prolactin in the observed alterations. Plasma osmolality (Posmol) and plasma sodium (PNa), similar in 8-day gravid and virgin Sprague-Dawley rats, decreased significantly by gestational day 10, reaching a nadir 8-10 mosmol/kg and 3-5 meq/l, respectively, below virgin levels by day 14 (both P less than 0.001). Despite this, plasma arginine vasopressin (PAVP) was measurable and similar in all pregnant and virgin groups. Osmotic thresholds for arginine vasopressin (AVP) secretion, similar in 8-day gravid and virgin rats, decreased 7.7 and 10.7 mosmol/kg in 12- and 14-day pregnant rats, respectively (both P less than 0.001). In contrast, Posmol decreased less than 2 mosmol/kg in 12- to 14-day pseudopregnant animals. When pseudopregnancy was prolonged to 18 days by prior hysterectomy, Posmol was only 2.6 mosmol/kg below that of cycling, hysterectomized controls. In other studies 14 days of hyperprolactinemia evoked by estradiol or treatment with ovine or rat prolactin had minimal effect on Posmol. We conclude that parallel decrements in Posmol and osmotic thresholds for AVP release occur during early rodent pregnancy, alterations that cannot be explained by gestational increases in circulating prolactin. In addition, the failure of pseudopregnancy. to mimic the hypotonicity of gestation suggests an important role for the fetoplacental unit in the osmoregulatory changes of rat pregnancy.

Animals↗
PubMed1988

Osmoregulation of thirst and vasopressin during normal menstrual cycle.

Changes in osmoregulation during normal menstrual cycle were examined in 15 healthy women. In 10 women, studied repetitively during two consecutive menstrual cycles, basal plasma osmolality, sodium, and urea decreased by 4 mosmol/kg, 2 meq/l, and 0.5 mM, respectively (all P less than 0.02) from the follicular to luteal phase. Plasma vasopressin, protein, hematocrit, mean arterial pressure, and body weight did not change. In five other women, diluting capacity and osmotic control of thirst and vasopressin release were assessed in follicular, ovulatory, and luteal phases. Responses of thirst and/or plasma vasopressin, urine osmolality, osmolal and free water clearance to water loading, and infusion of hypertonic saline were normal and similar in the three phases. However, the plasma osmolality at which plasma vasopressin and urine osmolality were maximally suppressed as well as calculated osmotic thresholds for thirst and vasopressin release were lower by 5 mosmol/kg in the luteal than in the follicular phase. This lowering of osmotic thresholds for thirst and vasopressin release, which occurs in the luteal phase, is qualitatively similar to that observed in pregnancy and should be taken into account when studying water balance and regulation of vasopressin secretion in healthy cycling women.

Adult↗
PubMed1993

Osmoregulation of the magnocellular system during pregnancy and lactation.

We compared the responsiveness of both the vasopressin (VP) and oxytocin (OT) magnocellular systems to osmotic stimulation during pregnancy and lactation to determine if changes in thresholds and sensitivities were similar for both neuropeptides. Virgin, pregnant (day 20), and lactating (day 6) Sprague-Dawley rats were injected with a hypertonic NaCl solution (0.25 M-8.0 M NaCl; 15 ml/kg sc) and decapitated 2 h later. Late in gestation, the apparent osmotic threshold for both VP and OT release was lower by approximately 10 mosmol/kgH2O than that of virgin and lactating animals. The sensitivity (i.e., slope of the linear regression relating plasma osmolality and VP or OT levels) of the magnocellular system to osmoregulation, however, was unchanged in pregnant animals but was significantly attenuated (P < 0.01) for both peptides during lactation (slopes of lactating vs. virgin rats: OT, 1.7 vs. 3.4; VP, 1.1 vs. 1.9). The neural lobe content of VP decreased (P < 0.05) in pregnant rats, whereas OT stores were reduced (P < 0.05) in lactating animals. Thus, during pregnancy, the lower tonicity of plasma is perceived as normal by both VP and OT neuroendocrine systems enabling excretion of an acute sodium or water load.

Animals↗
PubMed1997

Osmoregulation of the magnocellular neuroendocrine system during lactation.

Glucose utilization and Fos expression were used to compare responses of cerebral structures involved in osmoregulation in virgin and lactating rats given 0.15, 0.85, or 1.5 M NaCl subcutaneously. In virgin animals, glucose utilization increased (P < 0.05) in the supraoptic nuclei (SON), paraventricular nuclei (PVN), and neural lobe (NL) proportionally to the osmotic stimulus (0.15 M NaCl < 0.85 M NaCl < 1.5 M NaCl), whereas metabolism in the median preoptic nucleus (MPO) and median eminence (ME) increased only after 1.5 M NaCl. In lactating rats, enhanced utilization of glucose in response to osmotic stimulation was absent in the PVN (0.85 M NaCl), MPO, and ME or significantly (P < 0.01) reduced (SON, PVN, NL) compared with virgin animals. Glucose utilization in each structure correlated linearly with plasma osmolality but with a lower slope (P < 0.05) in lactating animals. Magnocellular neurons expressing Fos in the SON increased linearly with plasma osmolality and were more numerous (P < 0.05) in control lactating animals but increased less (P < 0.05) than in virgin rats after 0.85 M NaCl. The attenuated magnocellular response during lactation results from reduced afferent activation from osmosensitive forebrain sites.

Animals↗
PubMed1994

Osmoregulation at the Zoological Station of Naples at the end of the 19th century.

The Zoological Station of Naples was founded in 1872 by Anton Dohrn as a research institute for zoology and comparative anatomy. Although the original fields of interest were the morphology of vertebrates and comparative embryology, a department of physiology was added to the station in 1888. Osmoregulation in marine organisms has been extensively studied, notably by Bottazzi, who investigated chemical composition, electrical conductivity, surface tension, osmotic pressure and extracellular viscosity in circulating fluids in man and lower animals. Bottazzi classified aquatic animals into 2 groups, a distinction that is accepted today. More recent workers at the station include Bern, who made important contributions to the study of the essential role played by prolactin in regulation of hydromineral metabolism in euryhaline teleost fish in a freshwater environment.

Anatomy, Comparative↗
PubMed1981

Osmoregulation during pregnancy in the rat. Evidence for resetting of the threshold for vasopressin secretion during gestation.

Osmoregulation was studied in near term and age-matched Sprague-Dawley rats. Basal plasma osmolality (P(osm)) and plasma sodium (P(Na)) were 281+/-3 mosmol/kg and 134+/-3 meq/liter, respectively, on the 20th gestational day compared with 292+/-3 mosmol/kg and 140+/-1 meq/liter in virgin animals (P < 0.001), whereas P(urea) and plasma water content were similar in pregnant and control rats. These differences could not be reproduced in animals receiving progesterone, estrone, or a combination of progesterone and estradiol for 2 wk. Pregnant and control rats were deprived of water for periods ranging from 0 to 48 h. P(osm), always lower in gravidity, was 290+/-3 mosmol/kg after 2 d of water deprivation in pregnant animals compared with 300+/-2 mosmol/kg in controls (P < 0.001). Thus 48 h of dehydration were required before P(osm) in gravid rats was similar to basal values in the age-matched virgins. Despite strikingly lower P(osm), plasma arginine vasopressin (P(AVP)) and urinary osmolality (U(osm)) were similar in the basal state averaging 2.16+/-0.78 pg/ml and 1,652+/-406 mosmol/kg, respectively, during pregnancy compared with 2.08+/-2.17 pg/ml and 1,483+/-203 mosmol/kg in controls (NS). Water deprivation increased P(AVP) and U(osm) similarly in pregnant and virgin rats: these values reached 22.7+/-3.3 pg/ml and 3,300+/-123 mosmol/kg at 48 h in gravid compared with 26.0+/-6.4 pg/ml and 3,342+/-141 mosmol/kg in the controls (NS). Regression equations for P(AVP)vs. P(osm) which were highly significant (P < 0.001) in both groups demonstrated an apparent threshold for AVP secretion approximately 11 mosmol lower in gravid animals. Intravascular volume decreased, and plasma aldosterone increased during water deprivation, and both changes (Delta%) were significantly greater in the gravid animals (P <0.01). Therefore, P(osm) was increased without concomitant volume depletion by intraperitoneal hypertonic saline. Again P(AVP)vs. P(osm) correlated significantly (r > 0.9; P < 0.001) in each group, and the apparent threshold was 14 mosmol lower in pregnant animals. Diluting ability, tested by oral water loading, was not impaired in the pregnant animals which excreted a 30 ml/kg load as well as controls. Also, chronically hydrated virgin animals whose fluid intake was more than twice that of pregnant rats (for 19 d) did not lower their P(osm). In separate studies homozygous Brattleboro rats, which produce no endogenous vasopressin, were also shown to have a decreased P(osm) (pregnant 292+/-4 mosmol/kg; virgin 310+/-6 mosmol/kg P < 0.001), but unchanged U(osm) during pregnancy. Data demonstrate a resetting of the osmostat in gravid Sprague-Dawley rats as P(osm) and the threshold for AVP secretion both decrease significantly during gestation in this species. Studies in homozygous Brattleboro animals with hereditary diabetes insipidus suggest that the osmotic threshold for thirst is reset as well.

Animals↗
PubMed2005

The involvement of thyroid hormone metabolism in gilthead sea bream (Sparus auratus) osmoregulation.

We have investigated the effect of adaptation to low salinity water on the thyroid status of the euryhaline teleost, Sparus auratus. We show that, following low salinity adaptation, the plasma T(4) concentration increases and branchial deiodination activities of T(4), T(3), and rT(3) decrease. Moreover, branchial and hepatic enzyme activities that are putatively involved in thyroid hormone metabolism respond differentially in low salinity conditions. Our results indicate the involvement of thyroid hormones in Sparus auratus osmoregulation. Moreover, the gills appear well equipped to play an important role in the modulation of plasma thyroid hormone titers.

Adaptation, Physiological↗
PubMed1988

Taurine and osmoregulation: taurine is a cerebral osmoprotective molecule in chronic hypernatremic dehydration.

We studied the effect of 8-wk dietary taurine depletion on the vulnerability to hypernatremic dehydration in postweanling kittens. While experimental taurine depletion was not associated with increased susceptibility to acute hypernatremia (1.5 M NaCl/NaHCO3, 35 ml/kg body weight, single injection), there was an increase in mortality (five of seven versus one of seven, p = 0.05) and seizure activity (three of seven versus none of seven, p = 0.08) in taurine-depleted compared to taurine-replete kittens rendered chronically hypernatremic over 96 h. Furthermore, there was a significant decrease in brain cell water (517.4 +/- 21.7 versus 671.6 +/- 32.3 ml/100 g fat-free dry weight, p less than 0.05), derived almost exclusively from the intracellular compartment (352.5 +/- 12.3 versus 483.8 +/- 34.6 ml/100 g fat-free dry weight, p less than 0.05) that correlated with the reduction in the cerebral taurine content in the taurine-depleted versus control kittens during chronic hypernatremic dehydration. These results suggest that taurine is an important cerebral osmoprotective molecule. This aminoacid constitutes nearly 50% of the adaptable intracellular osmolal pool whose concentration varies in the course of osmoregulating in response to perturbations in the extracellular fluid tonicity.

Animals↗
PubMed1990

Taurine and osmoregulation. III. Taurine deficiency protects against cerebral edema during acute hyponatremia.

Taurine is a cerebral osmoprotective molecule during chronic hypernatremic dehydration. In these experiments, we investigated the role of taurine in osmoregulation during acute hyponatremia. Taurine deficiency was induced in experimental cats (n = 6) by feeding a taurine-free diet for 8-10 wk, whereas control counterparts (n = 6) consumed a regular diet. Hyponatremia was provoked in all cats over 54 h by daily injections of 5% dextrose in water (7.5% body wt) and vasopressin (20 U/d). The serum Na+ concentration was abruptly lowered to 110 +/- 3 and 117 +/- 2 mmol/L, in experimental and control animals, respectively. The cerebral total and intracellular water compartment sizes were reduced from 486 +/- 11 to 441 +/- 11 ml/100 g dry wt and from 357 +/- 7 to 309 +/- 12 mL/100 g dry wt, respectively, in control versus experimental cats, p less than 0.05. There was a significant linear relationship between cerebral taurine content and the intracellular water compartment size in all animals, p less than 0.02. Taurine displayed a similar osmoprotective capacity in muscle tissue in these studies. We conclude that taurine is an osmoregulatory molecule in cerebral and extracerebral tissues during severe hyponatremia. Reductions in tissue taurine content may complement decreases in cytosolic electrolyte levels during adaptation to more prolonged hyponatremia.

Animals↗
PubMed1984

Reduction of hypothalamic norepinephrine does not alter the osmoregulation of vasopressin in rats.

The supraoptic nuclei of the hypothalamus are known to be heavily innervated by noradrenergic neurons. However, the role of these neurons in regulating secretion of the antidiuretic hormone, arginine vasopressin, remains unsettled. In an effort to clarify this question, we studied the effect of multiple small doses of D,L alpha-methyl-p-tyrosine (alpha-MpT) on hypothalamic norepinephrine and the osmoregulation of vasopressin in rats. We found that, at the doses employed (80 mg/kg every 6 h for 24 h), alpha-Mpt reduced mean (+/- SD) hypothalamic norepinephrine by about 50% but did not affect plasma osmolality, sodium, glucose, urea, or vasopressin either under basal conditions or during osmotic stimulation by ip injection of hypertonic saline. During the latter, plasma vasopressin correlated directly with plasma osmolality and the regression lines that described the relationships in the control and drug-treated rats were identical. Hematocrit and mean arterial pressure were also unaffected by alpha-MpT. These findings do not support the concept based on previous studies that central noradrenergic pathways mediate the vasopressin response to osmotic stimuli.

Animals↗
PubMed1990

Osmoregulation of plasma vasopressin in myxedema.

We studied osmoregulation of plasma vasopressin (AVP) in eight patients with untreated myxedema due to primary hypothyroidism. All patients had severe thyroid hormone deficiency due to chronic thyroiditis and had been receiving no medication at the time of this study. AVP release was defined by 5% hypertonic saline infusion test in all patients, and urinary diluting capacity was estimated by the iv water-loading tests in five patients. Plasma AVP was measured by sensitive and specific RIA. The mean basal plasma AVP level in the patients (0.5 +/- 0.1 pmol/L) was significantly lower (P less than 0.01) than that in normal adults (2.5 +/- 0.5 pmol/L). During hypertonic saline infusion, the rise in plasma AVP was normal or subnormal in all patients. In two patients who showed mild to moderate hyponatremia in the basal state and mild urinary diluting defect during water loading, plasma AVP was appropriately suppressed in each case. These results indicate that inappropriate elevation of plasma AVP is not common in myxedema, and that impaired water excretion is due mainly to AVP-independent mechanisms.

Adult↗
PubMed2002

Osmoregulation in Paramecium: in situ ion gradients permit water to cascade through the cytosol to the contractile vacuole.

In vivo K(+), Na(+), Ca(2+) and Cl(-) activities in the cytosol and the contractile vacuole fluid of Paramecium multimicronucleatum were determined in cells adapted to a number of external osmolarities and ionic conditions by using ion-selective microelectrodes. It was found that: (1) under standardized saline conditions K(+) and Cl(-) were the major osmolytes in both the cytosol and the contractile vacuole fluid; and (2) the osmolarity of the contractile vacuole fluid, determined from K(+) and Cl(-) activities only, was always more than 1.5 times higher than that of the cytosol. These findings indicate that excess cytosolic water crosses the contractile vacuole complex membrane osmotically. Substitution of choline or Ca(2+) for K(+) in the external solution or the external application of furosemide caused concomitant decreases in the cytosolic K(+) and Cl(-) activities that were accompanied by a decrease in the water segregation activity of the contractile vacuole complex. This implies that the cytosolic K(+) and Cl(-) are actively coimported across the plasma membrane. Thus, the osmotic gradients across both the plasma membrane and the membrane of the contractile vacuole complex ensure a controlled cascade of water flow through the cell that can provide for osmoregulation as well as the possible extrusion of metabolic waste by the contractile vacuole complex.

Adaptation, Physiological↗