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PubMed1988

Light quality and osmoregulation in vicia guard cells : evidence for involvement of three metabolic pathways.

Osmoregulation in opening stomata of epidermal peels from Vicia faba L. leaves was investigated under a variety of experimental conditions. The K(+) content of stomatal guard cells and the starch content of guard cell chloroplasts were examined with cobaltinitrite and iodine-potassium iodide stains, respectively; stomatal apertures were measured microscopically. Red light (50 micromoles per square meter per second) irradiation caused a net increase of 3.1 micrometers in aperture and a decrease of -0.4 megapascals in guard cell osmotic potential over a 5 hour incubation, but histochemical observations showed no increase in guard cell K(+) content or starch degradation in guard cell chloroplasts. At 10 micromoles per square meter per second, blue light caused a net 6.8 micrometer increase in aperture over 5 hours and there was a substantial decrease in starch content of chloroplasts but no increase in guard cell K(+) content. At 25 micromoles per square meter per second of blue light, apertures increased faster (net gain of 5.7 micrometers after 1 hour) and starch content decreased. About 80% of guard cells had a higher K(+) content after 1 hour of incubation but that fraction decreased to 10% after 5 hours. In the absence of KCl in the incubation medium, stomata opened slowly in response to 25 micomoles per square meter per second of blue light, without any K(+) gain or starch loss. In dual beam experiments, stomata irradiated with 50 micomoles per square meter per second of red light for 3 hours opened without detectable starch loss or K(+) gain; addition of 25 micomoles per square meter per second of blue light caused a further net gain of 4.4 micometers in aperture accompanied by substantial K(+) uptake and starch loss. Comparison of K(+) content in guard cells of opened stomata in epidermal peels with those induced to open in leaf discs showed a substantially higher K(+) content in the intact tissue than in isolated peels. These results are not consistent with K(+) (and its counterions) as the universal osmoticum in guard cells of open stomata under all conditions; rather, the data point to sugars arising from photosynthesis and from starch degradation as additional osmotica. Biochemical confirmation of these findings would indicate that osmoregulation during stomatal opening is the result of three key metabolic processes: ion transport, photosynthesis, and sugar metabolism.

Journal Article↗
PubMed1987

Influence of nifedipine and enalapril on osmoregulation of vasopressin.

To determine whether calcium fluxes and angiotensin II influence osmoregulation of vasopressin (AVP) secretion, the effects of the calcium antagonist nifedipine and of the converting enzyme inhibitor enalapril on the AVP response to an osmotic load were compared to those of a placebo in seven normal female subjects. Plasma and urinary AVP were measured before and during a 3-h infusion of 2.5% hypertonic saline. Nifedipine (10 mg orally 2 h before and 10 mg at the start of the infusion) increased heart rate but did not change blood pressure. The changes in free water clearance and in urinary AVP induced by hypertonic saline under nifedipine were greater than in the control test, but the slope and the intercept of the regression line of plasma AVP upon plasma osmolality were not significantly different. Enalapril (10 mg 3 h before the infusion) did not change heart rate or blood pressure. Free water clearance and urinary AVP did not differ from the control test, but the slope of the regression line was less steep. These slight modifications of the response to an osmotic load suggest that calcium fluxes and angiotensin II only exert a limited influence on AVP osmoregulation in normal females.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1988

Osmoregulation of vasopressin secretion and thirst in cyclical oedema.

Osmoregulation of vasopressin release and thirst was studied in the mid-follicular and mid-luteal phases of the menstrual cycle of five patients with cyclical oedema defined by peripheral oedema and weight gain (greater than 3.0 kg) manifest in two consecutive luteal phases. Results are compared to those already obtained in eight healthy women. In the patients, basal plasma osmolality in the mid-luteal phase was significantly lower than in the mid-follicular periods (patients, 283 +/- 1, 287 +/- 1 mOsmol/kg, respectively, mean +/- SEM, P less than 0.05; controls, 282 +/- 1, 286 +/- 1 mOsmol/kg, respectively, P less than 0.05). Plasma osmolality (pOsm) and plasma arginine vasopressin (pAVP) were measured during hypertonic (850 mmol/l) saline infusion in both phases of the cycle; linear regression analyses of these data gave the following mean regression equations, (i) mid-follicular, pAVP = 0.55 (pOsm - 285), r = 0.94 and (ii) mid-luteal, pAVP = 0.42 (pOsm - 281), r = 0.93. The abscissal intercept was significantly different (P less than 0.025). Osmotic threshold for severe thirst onset was lower in the mid-luteal phase compared to the mid-follicular value (296 +/- 1, 299 +/- 1 mOsmol/kg, respectively, P less than 0.01). Basal data and results of thirst onset and theoretical threshold for vasopressin release in response to osmotic stimulation obtained in the patients were similar to healthy control women. We conclude that osmoregulation in cyclical oedema is normal.

Adult↗
PubMed1989

Osmoregulation of thirst and vasopressin secretion in Kallmann's syndrome.

It has been suggested that abnormalities of thirst and vasopressin secretion commonly coexist with Kallmann's syndrome. Out-patient plasma osmolality, plasma sodium and 24-hour urine volume were similar in 10 patients with Kallmann's syndrome and 10 matched controls. Six patients underwent dynamic testing of osmoregulation with hypertonic sodium chloride infusion. There were similar rises in plasma AVP concentration in patients (0.4 +/- 0.1-6.2 +/- 1.2 pmol/l, P less than 0.001) and controls (0.4 +/- 0.1-5.7 +/- 1.0 pmol/l P less than 0.001). Thirst ratings rose in similar fashion in patients (0.7 +/- 0.3-6.2 +/- 1.0 cm, P less than 0.001) and controls (1.0 +/- 0.3-7.2 +/- 0.5 cm. P less than 0.001). Drinking rapidly abolished thirst and lowered AVP concentrations in both groups before major changes in plasma osmolality occurred. Linear regression analysis defined similar osmotic thresholds for thirst onset and vasopressin release in the two groups, and there was no difference in the calculated sensitivity of the osmoreceptor/vasopressin secretory unit as defined by the slopes of the regression lines. We conclude that osmoregulation is normal in Kallmann's syndrome.

Adolescent↗
PubMed1991

The effect of a highly specific serotonin agonist on osmoregulated vasopressin secretion in healthy man.

OBJECTIVE: To explore a possible interaction of the serotonin neurotransmitter system and posterior pituitary function, we have looked at the effect of fluoxetine treatment on osmoregulated vasopressin secretion in normal men in two placebo controlled studies. DESIGN: In each study subjects took in random order for 7 days one capsule daily of placebo or 40 mg fluoxetine. On the 8th day subjects underwent assessment. Study 1 A hypo-osmotic stimulus of an oral water load of 20 ml/kg. Study 2 A hyperosmotic stimulus of intravenous infusion of 5% (855 mmol/l) saline at 0.06 ml/kg/min for 120 minutes. PATIENTS: Normal, healthy male volunteers. Study 1, 9; Study 2, 10. MEASUREMENTS: In both studies regular measures of plasma osmolality, sodium and vasopressin were made. In Study 1 urine osmolality was measured together with urine volume at set time points and an accumulative measure of percentage of water load excreted. Free water clearance was calculated. In Study 2 the relationship of plasma vasopressin to change in plasma osmolality was calculated for each subject by linear regression analysis. RESULTS: Serotonin agonism had no effect on baseline measurements in either study. Study 1 After 4 hours subjects excreted 95 and 99% of the water load after placebo and fluoxetine respectively (P = 0.407). There was no effect of fluoxetine compared to placebo on the pattern or extent of change of plasma osmolality (nadir 285.9 +/- 1.4 mosm/kg placebo, 283.1 +/- 1.1 mosm/kg fluoxetine, P = 0.145) or free water clearance or maximum urine dilution after oral water loading. Plasma vasopressin suppressed to a minimum concentration after both treatments in response to hypo-osmolality 0.5 +/- 0.1 pmol/l (placebo), 0.3 +/- 0.01 pmol/l (fluoxetine), P = 0.195. Study 2 Fluoxetine had no significant effect on the sensitivity of vasopressin release to change in plasma osmolality (0.33 +/- 0.06 pmol/l per mosm/kg placebo, 0.36 +/- 0.06 pmol/l per mosm/kg fluoxetine, P = 0.347). Nor was there a significant effect on the theoretical osmotic threshold for release of vasopressin (287.0 +/- 1.21 mosm/kg placebo, 286.9 +/- 1.09 mosm/kg fluoxetine, P = 0.700). CONCLUSION: We have found no evidence of a physiologically relevant effect of serotonin agonism on osmoregulated vasopressin release, or on the ability of normal man to excrete a water load. The possible reasons for this contrast to animal work are discussed.

Adolescent↗
PubMed1995

Promoter selectivity control of Escherichia coli RNA polymerase by ionic strength: differential recognition of osmoregulated promoters by E sigma D and E sigma S holoenzymes.

Transcription in vitro of two osmoregulated promoters, for the Escherichia coli osmB and osmY genes, was analysed using two species of RNA polymerase holoenzyme reconstituted from purified core enzyme and either sigma D (sigma 70, the major sigma in exponentially growing cells) or sigma S (sigma 38, the principal sigma at stationary growth phase). Under conditions of low ionic strength, the osmB and osmY promoters were transcribed by both E sigma D and E sigma S. Addition of up to 400 mM potassium glutamate (K glutamate), mimicking the intracellular ionic conditions under hyperosmotic stress, specifically enhanced transcription at these promoters by E sigma S but inhibited that by E sigma D. At similar high concentrations of potassium chloride (KCl), however, initiation at both these promoters was virtually undetectable. These data suggest that the RNA polymerase, E sigma S, itself can sense osmotic stress by responding to changes in intracellular K glutamate concentrations and altering its promoter selectivity in order to recognize certain osmoregulated promoters.

DNA-Directed RNA Polymerases↗
PubMed1997

Efflux of compatible solutes in Corynebacterium glutamicum mediated by osmoregulated channel activity.

Bacteria respond to hypoosmotic stress by releasing low-molecular-mass solutes in order to maintain constant turgor pressure. We have studied the function of osmoregulated channel(s) in Corynebacterium glutamicum, which are responsible for efflux of various solutes upon sudden decrease in osmotic pressure. The channels preferentially mediated efflux of compatible solutes such as glycine betaine and proline. The release of molecules of similar size, e.g. glutamate or lysine, was restricted, ATP was completely retained even after severe osmotic shock. The cells maintained high cytoplasmic K+ and Na+ concentrations under hypoosmotic shock. Several results suggest that the solute efflux is mediated by a channel and not by a carrier, e.g. by reversal of the glycine betaine uptake systems of C. glutamicum: the release of glycine betaine and proline was extremely fast reaching an efflux rate of 6000 micromol x min(-1) x g dm(-1) or higher; the efflux was not significantly influenced by addition of external transport substrate, e.g. glycine betaine; in spite of an extremely high chemical gradient, no significant efflux under isoosmolar conditions was observed; efflux of solutes was unchanged after full uncoupling of membrane energetics by carbonylcyanide m-chlorophenylhydrazone (CCCP). These results indicate the presence of an osmoregulated channel in C. glutamicum similar to the mechanosensitive channel(s) of Escherichia coli. The activity of the channel did not depend on the growth conditions, but we observed a tight regulation on the level of activity, i.e. the mechanosensitive channel behaved as a perfect osmometer. By monitoring release of glycine betaine under slow and continuous decrease of the external osmolality, we observed continous efflux whithout a stepwise release of solutes. This resulted in a significant steady-state decrease of the membrane potential.

Adenosine Triphosphate↗
PubMed2002

The substrate-binding protein TeaA of the osmoregulated ectoine transporter TeaABC from Halomonas elongata: purification and characterization of recombinant TeaA.

TeaABC is a novel, osmoregulated secondary transport system for compatible solutes found in the halophilic proteobacterium Halomonas elongata DSM 2581(T). Sequence comparisons have confirmed that TeaABC belongs to the family of TRAP transporters and as such it consists of two putative transmembrane proteins (TeaB, TeaC) and a putative periplasmic substrate-binding protein (TeaA). TeaABC is the only osmoregulated transporter for ectoines found in H. elongata. By overexpressing TeaA-(6)His tag in Escherichia coli we demonstrated that TeaA is processed as predicted and exported to the periplasm. Furthermore, it was proven that TeaA is indeed a periplasmic ectoine-binding protein. The functionality of the purified protein as an ectoine-binding protein was tested employing a modified binding assay.

Amino Acid Sequence↗
PubMed1984

envZ mediates transcriptional control by local anesthetics but is not required for osmoregulation in Escherichia coli.

Expression of a particular set of exported protein genes (ompF, ompC, phoA, and malE) can be specifically altered in three ways: variation in the osmotic strength of the growth medium, mutations in the regulatory locus envZ, or treatment with sublethal concentrations of the local anesthetic procaine. To clarify relationships among these factors in the regulation of transcription, expression of the affected genes was compared in envZ+ and envZ22(Am) mutant strains grown in media of differing osmolarities with and without procaine. Loss of the envZ product resulted in complete resistance of gene expression to procaine, supporting the hypothesis that envZ mediates procaine inhibition. The specific activity of the phoA product, alkaline phosphatase, was elevated in envZ22 mutant strains, while the amounts of both the OmpC and OmpF porins were reduced. Osmotic control of phoA and ompC was retained in the absence of envZ function, but osmoregulation of ompF was lost. Therefore, the envZ product is somehow involved in the complex regulation of all four target genes, but is not solely responsible for osmoregulation.

Bacterial Proteins↗
PubMed1986

cis-acting sites required for osmoregulation of ompF expression in Escherichia coli K-12.

OmpF and OmpC are major outer membrane proteins which form passive diffusion pores in Escherichia coli K-12. The expression of the structural genes for these proteins, ompF and ompC, is influenced by medium osmotic strength and requires the products of two regulatory genes, ompR and envZ. We have constructed a series of ompF-lacZ fusions containing different regions of ompF to determine sites involved with osmoregulation. These fusions were crossed onto a specialized transducing phage and integrated into the bacterial chromosome in unit copy. By measuring the fluctuations of beta-galactosidase activity in lysogens grown in high versus low osmolarity, we have identified three regions which are necessary. Furthermore, we have determined that, although the OmpR activation site is not sufficient, OmpR is probably essential for ompF osmoregulation.

Bacterial Outer Membrane Proteins↗
PubMed1988

Altered osmoregulation of ompF in integration host factor mutants of Escherichia coli.

Osmoregulation of the porin protein OmpF was strongly altered in integration host factor (IHF) mutants. These mutants produced approximately 15-fold more OmpF than did the parent strain when grown in media of intermediate osmolarity. At high osmolarity IHF mutants continued to produce considerable amounts of OmpF, although this protein was undetectable in the parent grown under these conditions. Experiments with an ompF-lacZ chromosomal fusion strain suggested that these changes in osmoregulation in large part involve alterations in transcriptional activity of the ompF promoter. These results add to the growing list of genes whose expression is modified in IHF mutants.

Bacterial Outer Membrane Proteins↗
PubMed1988

Rapid response to osmotic upshift by osmoregulated genes in Escherichia coli and Salmonella typhimurium.

The rapid in vivo response of both Escherichia coli and Salmonella typhimurium osmoregulated genes to an osmotic upshift was analyzed in detail by using chromosomal operon fusions. Within 10 min after the addition of 0.3 M NaCl to the culture medium, the differential rates of expression of both an S. typhimurium proU-lac fusion and a proP-lac fusion increased by 180- and 17-fold respectively, while an E. coli ompC-lac fusion increased by 3.4-fold. For all three stimulated promoters, the increased rate of expression was maintained until about 40 min after the osmotic upshift. Thereafter, proU expression continued at a steady-state rate that was 27-fold higher than that of the control, while proP and ompC expression fell to 1.4- and 2-fold of the control rates, respectively. In contrast, expression of an E. coli ompF-lac fusion decreased twofold within 2.5 min. For proU, the length of the lag phase, which preceded the onset of the rapid response, increased with the degree of osmotic upshift, above a threshold of 0.2 M NaCl; the onset of the rapid proU response also preceded the resumption of growth. The rapid response phase, which was first quantitated for proU, proP, ompC, and ompF in this study, is an important component of the osmoregulation of these promoters. The addition of the osmoprotectant glycine betaine at the time of osmotic upshift decreased both the length of the rapid response and the subsequent steady-state of expression of proU.

Bacterial Outer Membrane Proteins↗
PubMed2001

Osmoregulated periplasmic glucans of Erwinia chrysanthemi.

We report the initial characterization of the osmoregulated periplasmic glucans (OPGs) of Erwinia chrysanthemi. OPGs are intrinsic components of the bacterial envelope necessary to the pathogenicity of this phytopathogenic enterobacterium (F. Page, S. Altabe, N. Hugouvieux-Cotte-Pattat, J.-M. Lacroix, J. Robert-Baudouy and J.-P. Bohin, J. Bacteriol. 183:0000-0000, 2001 [companion in this issue]). OPGs were isolated by trichloracetic acid treatment and gel permeation chromatography. The synthesis of these compounds appeared to be osmoregulated, since lower amounts of OPGs were produced when bacteria were grown in media of higher osmolarities. However, a large fraction of these OPGs were recovered in the culture medium. Then, these compounds were characterized by compositional analysis, high-performance anion-exchange chromatography, matrix-assisted laser desorption mass spectrometry, and (1)H and (13)C nuclear magnetic resonance analyses. OPGs produced by E. chrysanthemi are very heterogeneous at the level of both backbone structure and substitution of these structures. The degree of polymerization of the glucose units ranges from 5 to 12. The structures are branched, with a linear backbone consisting of beta-1,2-linked glucose units to which a variable number of branches, composed of one glucose residue, are attached by beta-1,6 linkages in a random way. This glucan backbone may be substituted by O-acetyl and O-succinyl ester-linked residues.

Chromatography, Ion Exchange↗
PubMed2002

New type of osmoregulated solute transporter identified in halophilic members of the bacteria domain: TRAP transporter TeaABC mediates uptake of ectoine and hydroxyectoine in Halomonas elongata DSM 2581(T).

The halophilic bacterium Halomonas elongata synthesizes as its main compatible solute the aspartate derivative ectoine. We constructed a deletion mutant of H. elongata, KB1, defective in ectoine synthesis and tolerating elevated salt concentrations only in the presence of external compatible solutes. The dependency of KB1 on solute uptake for growth in high-salt medium was exploited to select insertion mutants unable to accumulate external solutes via osmoregulated transporters. One insertion mutant out of 7,200 failed to accumulate the osmoprotectants ectoine and hydroxyectoine. Genetic analysis of the insertion site proved that the mutation affected an open reading frame (ORF) of 1,281 bp (teaC). The nucleotide sequence upstream of teaC was determined, and two further ORFs of 603 bp (teaB) and 1,023 bp (teaA) were identified. Deletion of teaA and teaB proved that all three genes are mandatory for ectoine uptake. Sequence comparison showed significant identity of TeaA, TeaB, and TeaC to the transport proteins of the recently identified tripartite ATP-independent periplasmic transporter family (TRAP-T). The affinity of the cells for ectoines was determined (K(s) = 21.7 microM), suggesting that the transporter TeaABC exhibits high affinity for ectoines. An elevation of the external osmolarity resulted in a strong increase in ectoine uptake via TeaABC, demonstrating that this transporter is osmoregulated. Deletion of teaC and teaBC in the wild-type strain led to mutants which excreted significant amounts of ectoine into the medium when cultivated at high salt concentrations. Therefore, the physiological role of TeaABC may be primarily to recover ectoine leaking through the cytoplasmic membrane.

Acetyltransferases↗
PubMed1990

An emerging role for a cardiac peptide hormone in fish osmoregulation.

It is clear from the extant literature that various fish groups face chronic osmoregulatory problems that depend on the surrounding salinity. Their physiologic and hormonal responses are largely those seen in the mammals, but their terrestrial descendants have lost osmoregulatory structures such as gills and rectal glands and depend primarily on renal function. A data base is now emerging that strongly suggests that a putative atriopeptin plays a role in osmoregulation in fishes. This conclusion is supported by the fact that heterologous AP produces relevant physiologic responses (e.g. natriuresis, vasodilation, stimulation, or inhibition of Na+ secretion by intestine, gills, and rectal gland) in both teleosts and elasmobranchs. Moreover, cardiac and brain extracts from fish can produce similar effects in both fishes and mammals, and these tissues from various fish groups contain immunoreactive AP, as does plasma. Both physiologic and immunologic evidence suggests that the ventricle may be a significant source of AP in fishes, contrary to the situation in mammals. Finally, osmotic perturbations result in a change in plasma and tissue APir levels. The finding that plasma APir levels increase in sea water, and that heterologous AP stimulates salt secretion by the teleost gill and shark rectal gland, and inhibits salt uptake by the teleost intestine, suggests that AP may primarily play a role in salt, rather than fluid, secretion in fishes. The fact that in mammals AP inhibits prolactin secretion, but is itself stimulated by cortisol, supports this conclusion, since prolactin is generally considered to be the dominant osmoregulatory hormone in freshwater fishes, and cortisol serves this function in marine fishes. In addition, if AP inhibits brain AVT release in fishes, as it apparently inhibits vasopressin release in mammals, this also would be adaptive in marine fishes since AVT in fishes is diuretic, rather than antidiuretic. Interactions between AP and these hormones (prolactin, cortisol, and ATV) have not been studied in fishes to date, but these theoretical interactions do lend support to the hypothesis that AP may function primarily in salt homeostasis in fishes. At least one potential hormonal interaction counters this argument, however. Atriopeptin is known to inhibit the production and effects of angiotensin II in mammals, and since this hormone is apparently dipsogenic in fishes, it may play a critical role in osmoregulation in sea water. Finally, it is of some historical interest that in Keys' (67) original description of the eel heart-gill perfusion system in 1931 he commented that gill resistance remained constant for hours only if the heart itself was perfused.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

Osmoregulation of glycerophosphorylcholine content of mammalian renal cells.

Renal medullary cells contain high concentrations of "compatible" organic osmolytes such as glycerophosphorylcholine (GPC), betaine, myo-inositol, and sorbitol. The organic osmolytes occur as an osmoregulatory response to the high and variable interstitial NaCl concentration that is part of the urinary concentrating mechanism. Madin-Darby canine kidney (MDCK) cells in culture were previously shown to accumulate GPC in response to increased osmolality. We demonstrate here that this accumulation occurs in response to elevated extracellular urea concentration as well as to elevated NaCl. GPC does not accumulate unless either choline or GPC is present in the medium. Thus the accumulation results from osmoregulated synthesis of GPC from choline and, possibly, also osmoregulated uptake of extracellular GPC. When the osmolality is decreased from high to normal levels, cell GPC concentration decreases greatly over 24 h, accompanied by efflux of GPC and choline into the medium.

Animals↗
PubMed1986

Effect of ovarian sex steroids on osmoregulation and vasopressin secretion in the rat.

Effects of sex steroids on osmoregulation were studied in intact and ovariectomized Sprague-Dawley rats treated for 2 wk with subcutaneously implanted hormone pellets containing 0.5 mg 17 beta-estradiol (E2) alone (group 1) or combined with 50 mg progesterone (PG; group 2) and 5.0 mg E2 alone (group 3) combined with PG (group 4). An additional group (5) of animals was given 14 daily injections with 100 micrograms/100 g body weight of E2. Controls for each group received vehicle alone. There were no alterations in basal plasma osmolality (Posmol) or vasopressin (PAVP), except for group 3 in which a small (2.5 mosmol/kg) decrement in Posmol was observed. However, mean PNa was decreased (0.9-3.4 meq/l) in hormone-treated rats, and alterations in Pglucose and/or Purea could not explain the Na-osmolal discrepancy. Intraperitoneal hypertonic saline resulted in stepwise increases in both Posmol and PAVP. Regression analysis of PAVP on Posmol demonstrated similar osmotic thresholds for AVP release in estrogen and control rats, but the slope (sensitivity of the response) was significantly (P less than 0.005) greater in hormone-treated animals. In contrast, the PAVP response to isosmotic volume depletion was not altered by estrogen. The enhanced response to osmotic stimuli could not be explained by alterations in plasma volume or pituitary AVP content and differed from PAVP -Posmol relationships observed by us previously in gravid rats. In other experiments Posmol and PAVP were similar during all stages of the estrus cycle, while Posmol was approximately equal to 10 mosmol/kg lower in 21-day gravid rats. These data demonstrate that, although estradiol has little effect on basal osmoregulation or hemodynamically mediated AVP release, PAVP responses to osmotic stimuli are markedly enhanced. These osmoregulatory effects, however, differ from those observed during rodent gestation.

Animals↗
PubMed1987

Effect of insulin on osmoregulation of vasopressin.

Patients with uncontrolled insulin-dependent diabetes mellitus have elevations in plasma vasopressin that cannot be completely accounted for by recognized stimuli. To determine whether insulin deficiency per se increases plasma vasopressin, we investigated the effect of acute insulin depletion on the osmoregulation of plasma vasopressin in insulin-dependent diabetics. When intravenous insulin infusion was stopped, plasma vasopressin, osmolality, and glucose increased over the ensuing 5 h, whereas plasma sodium decreased, and blood volume and pressure did not change. This increase in vasopressin was not due to a loss of osmoregulation, because changes in plasma osmolality and sodium, induced by infusion of hypertonic saline or water loading, induced appropriate vasopressin responses under insulin deplete as well as replete conditions. However, when plasma osmolality and glucose were raised by infusion of hypertonic dextrose, plasma vasopressin increased significantly in diabetic patients under insulin-deplete but not under insulin-replete conditions and actually decreased in healthy controls. These results indicate that acute insulin depletion increases vasopressin secretion by sensitizing the osmoreceptor to stimulation by hyperglycemia. This change in osmoreceptor specificity may be explained by postulating that glucose transport by osmoreceptor neurons as insulin dependent.

Adult↗