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PubMed1973

Stimulation by vasopressin of glycogen breakdown and gluconeogenesis in the perfused rat liver.

1. Vasopressin (anti-diuretic hormone, [8-arginine]vasopressin) stimulated the breakdown of glycogen in perfused livers of fed rats, at concentrations (50-600muunits/ml) that have been reported in the blood of intact rats, especially during acute haemorrhagic shock. 2. In perfused livers from starved rats, vasopressin (30-150muunits/ml) stimulated gluconeogenesis from a mixture of lactate, pyruvate and glycerol. 3. Vasopressin prevented accumulation of liver glycogen in the perfused liver of starved rats, or in starved intact rats. 4. The action of vasopressin on hepatic carbohydrate metabolism thus resembles that of glucagon; the minimum effective circulating concentrations of these hormones are of the same order (100pg/ml). 5. The stimulation of hepatic glucose output by vasopressin is discussed in connexion with the release of glucose and water from the liver.

Animals↗

PubMed1981

Stimulation of hepatic lipogenesis and acetyl-coenzyme A carboxylase by vasopressin.

The effect of vasopressin on the short-term regulation of fatty acid synthesis was studied in isolated hepatocytes from rats fed ad libitum. Vasopressin stimulates fatty acid synthesis by 30-110%. This increase is comparable with that obtained with insulin. Angiotensin also stimulates fatty acid synthesis, whereas phenylephrine does not. The dose-response curve for vasopressin-stimulated lipogenesis is similar to the dose-response curve for glycogenolysis and release of lactate plus pyruvate. Vasopression also stimulates acetyl-CoA carboxylase activity in a dose-dependent manner. Vasopressin does not relieve glucagon-inhibited lipogenesis, whereas insulin does. The action of vasopressin on hepatic lipogenesis is decreased, but not suppressed, in Ca2+-depleted hepatocytes. The results suggest that vasopressin acts on lipogenesis by increasing availability of lipogenic substrate (lactate + pyruvate) and by activating acetyl-CoA carboxylase.

Acetyl-CoA Carboxylase↗

PubMed1984

Distinct effects of glucagon and vasopressin on proline metabolism in isolated hepatocytes. The role of oxoglutarate dehydrogenase.

The hormonal regulation of gluconeogenesis and ureogenesis in isolated rat hepatocytes with 5 mM-proline as precursor was studied, with the following results. (1) The formation of glucose and urea in a 30 min interval were stimulated more by vasopressin than by glucagon, and the effects of the two hormones in combination were additive. (2) The rates of gluconeogenesis during the 30 min were constant under control, glucagon-stimulated and glucagon-plus-vasopressin-stimulated conditions. The stimulated rate in the presence of vasopressin diminished with time; glucagon in combination with vasopressin prevented this diminution, resulting in an additive effect. (3) Coincident with these changes in gluconeogenesis, vasopressin caused a decrease in cell oxoglutarate concentration, which, in contrast with the decrease caused by glucagon, was greater, but not sustained unless glucagon was also present. Changes in cell glutamate concentration similar to those observed for oxoglutarate occurred. (4) The data suggest that activation of oxoglutarate dehydrogenase (EC 1.2.4.2) by glucagon and vasopressin by different mechanisms may explain the relative effects of the hormones alone and in combination on gluconeogenesis from proline.

Amino Acids↗

PubMed1986

Stimulation, by vasopressin and other agonists, of inositol-lipid breakdown and inositol phosphate accumulation in WRK 1 cells.

WRK 1 cells were labelled to equilibrium with 2-myo-[3H]inositol and stimulated with vasopressin. Within 3 s of hormone stimulation there was a marked accumulation of 3H-labelled InsP2 and InsP3 (inositol bis- and tris-phosphate), but not of InsP (inositol monophosphate). There was an associated, and rapid, depletion of 3H-labelled PtdInsP and PtdInsP2 (phosphatidylinositol mono- and bis-phosphates), but not of PtdIns (phosphatidylinositol), in these cells. Some 4% of the radioactivity in the total inositol lipid pool of WRK 1 cells was recovered in InsP2 and InsP3 after 10 s stimulation with the hormone. The selectivity of the vasopressin receptors of WRK 1 cells for a variety of vasopressin agonists and antagonists revealed these to be of the V1a subtype. There was no receptor reserve for vasopressin-stimulated inositol phosphate accumulation in WRK 1 cells. The accumulation of inositol phosphates was enhanced in the presence of Li+ions. Half-maximal accumulation of InsP, InsP2 and InsP3 in vasopressin-stimulated cells was observed with 0.9, 3.0 and 3.6 mM-Li+ respectively. Bradykinin and 5-hydroxytryptamine also provoked inositol phosphate accumulation in WRK 1 cells. The effects of sub-optimal concentrations of bradykinin and vasopressin upon inositol phosphate accumulation were additive, but those of optimal concentrations of the hormones were not.

Animals↗

PubMed1988

Activation of rat liver plasma-membrane diacylglycerol kinase by vasopressin and phenylephrine.

Plasma-membrane fractions were prepared from the livers of rats injected with 0.15 M-NaCl (controls) or vasopressin (1 nmol/kg body wt.). When assayed in the presence of deoxycholate, vasopressin increased the Vmax. of plasma-membrane diacylglycerol kinase 2-4-fold, and the apparent Km of the enzyme for 1,2-dioleoyl-sn-glycerol was doubled. The effect of vasopressin on the Vmax. of plasma-membrane diacylglycerol kinase was twice as great between pH 7 and 8.5 than at pH 6 or 6.5. Vasopressin doubled the activity of diacylglycerol kinase in the plasma-membrane fraction when the enzyme was assayed with phosphatidylserine rather than deoxycholate as stimulator, and when either 1-stearoyl-2-arachidonoyl-sn-glycerol or 1,2-dioleoyl-sn-glycerol was the substrate. In perfused livers vasopressin (10 nM) increased the Vmax. of plasma-membrane diacylglycerol kinase 2-fold, and phenylephrine (3 microM) gave a similar effect. Vasopressin doubled diacylglycerol kinase activity in hepatocytes that had been preincubated for 55 min, but not in cells that had only been preincubated for 15 min.

Animals↗

PubMed1988

Epidermal growth factor stimulates phospholipase A2 in vasopressin-treated rat glomerular mesangial cells.

Epidermal growth factor (EGF) enhances vasopressin- and ionophore-A23187-induced prostaglandin production and arachidonate release by rat glomerular mesangial cells in culture. The purpose of the present study was to delineate the phospholipid pathways involved in this effect. In cells labelled with [14C]arachidonate, EGF significantly enhanced the free arachidonate released in response to A23187 or vasopressin without enhancing the production of [14C]arachidonate-labelled diacylglycerol. EGF increased the [14C]arachidonate-labelled phosphatidic acid formed in response to vasopressin, but to a much smaller extent than it increased free arachidonate release. These results indicate that activation of phospholipase C is not sufficient to explain the increase in free arachidonate release observed on addition of EGF. To examine if EGF enhanced phospholipase A2 activity, mesangial cells were labelled with [2-2H]glycerol and [14C]-arachidonate, and the formation of arachidonate-poor lysophospholipids was studied. When combined with vasopressin, EGF significantly enhanced the formation of arachidonate-poor lysophospholipids as compared with vasopressin alone. The fate of exogenously added lysophosphatidylcholine was not altered after stimulation with vasopressin plus EGF, indicating that decreased deacylation or reacylation of the lysophospholipids was not responsible for their accumulation. Taken together, these results indicate that EGF enhances free arachidonate release by activation of phospholipase A2. The signalling mechanism responsible for the change in phospholipase A2 activity is not known, but could conceivably involve phosphorylation of modulating proteins such as lipocortin or G-proteins.

Animals↗

PubMed1989

Exposure of cultured hepatocytes to cyclic AMP enhances the vasopressin-mediated stimulation of inositol phosphate production.

Isolated rat hepatocytes in primary monolayer culture were maintained for 18-24 h in the presence of 10% (v/v) serum and [3H]inositol. Vasopressin (100 nM) stimulated the production of inositol mono-, bis- and tris-phosphates (IP1, IP2, and IP3). Prior exposure of hepatocytes to 8-bromo cyclic AMP (8Br-cAMP; 100 microM), but not 8-bromo cyclic GMP, enhanced the vasopressin-mediated stimulation of inositol phosphate accumulation, but had no significant effect on their formation in the absence of vasopressin. The effect of the cyclic AMP analogue was mimicked by glucagon (10 nM), and was seen whether cyclic AMP or glucagon was added 5 min or 12 h before the addition of vasopressin. An 8 h incubation with dexamethasone (100 nM) enhanced the accumulation of IP3, but not that of IP2 or IP1, in the presence of 8Br-cAMP and vasopressin. Cycloheximide or actinomycin D had little effect on the vasopressin stimulation of inositol phosphate accumulation, after an 8 h incubation in the presence or absence of 8Br-cAMP.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1976

Effect of vasopressin on uric acid excretion: evidence for distal nephron reabsorption of urate in man.

1. When changes in urine flow rate were induced by vasopressin administration in eight subjects, urate excretion decreased by a mean of 14% and was positively correlated with urine flow rate (r = 0.88, P less than 0.01). The effect of vasopressin on urate excretion was not influenced by prior changes in extracellular fluid volume. 2. Mannitol administration in a dose sufficient to prevent vasopressin-induced alterations in urine flow rate blocked the effect of vasopressin on urate excretion. 3. Alterations in urate excretion produced by changes in extracellular fluid volume could be distinguished from the urate-retaining effect of vasopressin-mediated decrease in urine flow. Urate retention after vasopressin was entirely attributed to a decrease in pyrazinamide-suppressible urate excretion, consistent with either decreased secretion or enhanced post-secretory reabsorption of urate. 4. Since diminished urine flow rate in the distal part of the nephron is more likely to lead to enhanced reabsorption of urate, these results provide additional evidence for urate reabsorption in the distal part of the nephron.

Adult↗

PubMed1980

Fate of vasopressin perfused into nephrons of Wistar and Brattleboro (diabetes insipidus) rats.

1. Iodinated vasopressin was microinjected into early proximal or distal tubules or Wistar and Brattleboro (diabetes insipidus) rats. Sites of infusion were determined by the lissamine green transit time method. 2. Urinary recovery of 125I after proximal and distal injections was 89 +/- SE 1.7% and 94 +/- 1.0% in Wistar rats (corrected for inulin) and 81 +/- 2.0 and 92 +/- 2.0% in Brattleboro rats (uncorrected); injection of hormone into vascular stars resulted in similar 125I recoveries from punctured and contralateral kidneys. 3. Radioactive substances excreted after perfusing proximal and distal sites in Brattleboro animals, and 125I-labelled hormone added to urine from the contralateral kidney, bound similarly to a specific arginine vasopressin antiserum and demonstrated similar radioactive elution profiles after passage through Sephadex G25 columns. 4. Incubation of labelled and unlabelled vasopressin with rat kidney homogenates resulted in similar and complete degradation of the hormone. 5. Results indicate that most of the vasopressin injected into either proximal or distal nephrons enters the urine intact, and no evidence of tubular secretion was found when perfusing vascular stars. Enzymes in rat renal tissue degrade labelled vasopressin, but the ability of the proximal tubule to hydrolyse the 125I-labelled vasopressin is limited, especially when compared with that reported for several linear peptide hormones.

Animals↗

PubMed1980

Immunocytochemical localization of angiotensin II and vasopressin in rat hypothalamus: evidence for production in the same neuron.

1. By immunoperoxidase technique, immunoreactive angiotensin II (ANG II) was located in the cell bodies of many magnocellular neurons in the supraoptic and paraventricular nuclei of the hypothalamus and their pathways to median eminence and posterior pituitary gland in the rat. 2. Like vasopressin and its neurophysin, but not oxytocin, ANG II was also found in parvocellular neurons in the suprachiasmatic nucleus. 3. Analysis of these peptides in the same magnocellular neurons reveals that ANG II is localized primarily in vasopressin cells. 4. Like vasopressin and its precursor, ANG II is deficient in homozygous Brattleboro rats with diabetes insipidus. 5. In adrenalectomized rats increases in vasopressin and its neurophysin in median eminence are associated with increases in ANG II. 6. The data suggest that the ANG II demonstrated shares antigenic determinants with the vasopressin precursor, or is regulated in a similar way to vasopressin in the same neurons.

Adrenalectomy↗

PubMed1981

Vasopressin in the plasma of stroke-prone spontaneously hypertensive rats.

1. Plasma concentration of arginine vasopressin, plasma osmolality and packed cell volume were measured in stroke-prone spontaneously hypertensive rats (SHRSP) and in normotensive Wistar-Kyoto (WKY) rats at different ages. 2. In young and in adolescent SHRSP, at 6, 9 and 12 weeks of age, plasma concentration of vasopressin was diminished as compared with age-matched WKY rats (P less than 0.01), whereas, in 18-week-old rats, the difference was not significant (P greater than 0.05). In contrast, in 24-week-old rats, plasma vasopressin was elevated as compared with WKY rats of the same age (P less than 0.01). 3. In none of the age groups did plasma osmolality differ between the two strains of rats, but in all groups packed cell volume in SHRSP was higher than in WKY rats. 4. During a 48 h period of dehydration, plasma vasopressin concentrations increased similarly in SHRSP and in WKY rats of 6 and 12 weeks of age respectively. 5. It is concluded that vasopressin does not contribute to the development of high blood pressure in SHRSP rats. The reduced plasma concentration of vasopressin may account for the decreased plasma and blood volume and the slightly elevated plasma sodium concentration observed in young SHRSP rats.

Animals↗

PubMed1981

The reflex control of arginine-vasopressin release in essential hypertension.

1. The reflex control of arginine-vasopressin release was studied in 12 essential established hypertensive patients and in 12 age-matched normal subjects by comparing the effects of head-up tilt and a variable-pressure neck-chamber. 2. After 45 min 85 degrees head-up tilt, normal subjects showed an increase in plasma arginine-vasopressin and in plasma renin activity, while plasma volume decreased. In hypertensive patients, plasma arginine-vasopressin showed changes after tilt opposite to those of controls, while the changes in plasma renin activity and plasma volume were similar to those observed in the normal group. In both groups the changes in systolic and diastolic blood pressure were not statistically significant. A reduction in carotid sinus transmural pressure obtained by increasing neck-tissue pressure (+50 mmHg) by means of a neck-chamber, evoked different responses in mean blood pressure in the two groups, but failed to induce any significant change in plasma arginine-vasopressin concentration both in the normal and in the hypertensive subjects. 3. These results seem to suggest that carotid sinus baroreceptors, though active in blood pressure control, do not play a direct role in arginine-vasopressin release and, therefore, the opposite response of arginine-vasopressin observed after tilt in the two groups of subjects should be ascribed to more complex mechanisms.

Adolescent↗

PubMed1985

A vasopressin-mediated diminution of potassium excretion in water-loaded man.

Intravenous vasopressin (1-3 mu-units min-1 kg-1) had an antidiuretic effect on water-loaded man and also diminished potassium excretion. As noted by others, aspirin (2.4 g) enhanced the antidiuretic effect of vasopressin, but the fall in potassium excretion was not modified by prior administration of aspirin, which makes it unlikely that the fall was due to the release of endogenous prostaglandins. After terminating the infusion of vasopressin, the fall in potassium output persisted longer than the antidiuresis, which makes it unlikely that the antikaliuretic effect of vasopressin is secondary to its effect on urine flow. The unchanged antikaliuretic effect of vasopressin after aspirin treatment, together with its persistence after terminating the infusion, suggest the possible existence of vasopressin-mediated potassium absorption in the distal nephron in certain circumstances. Aspirin administration had specific effects of its own in water-loaded man. It decreased both the water diuresis and sodium excretion but did not alter potassium excretion or urine osmolality.

Adult↗

PubMed1986

The osmotic thresholds for thirst and vasopressin release are similar in healthy man.

The relationship between thirst perception and plasma osmolality was studied during hypertonic and physiological saline infusion in ten healthy volunteers. Thirst perception was quantified using a linear visual analogue scale which volunteers marked at intervals during the infusion periods. Infusion of hypertonic saline caused a steady rise in plasma osmolality together with a progressive linear increase in thirst perception and also plasma arginine vasopressin. No significant changes in thirst, plasma osmolality or plasma arginine vasopressin occurred during infusion of physiological saline. Linear regression analysis of the results defined the functions. Thirst (cm) = 0.3 (plasma osmolality-281) (r = +0.92, P less than 0.001) and plasma arginine vasopressin (pmol/l) = 0.4 (plasma osmolality-285) (r = +0.96, P less than 0.001). The osmolar threshold for thirst onset thus defined (281 mosmol/kg) was much lower than in previous studies and similar to the theoretical osmolar threshold for vasopressin release (285 mosmol/kg). We conclude that thirst perception rises in a progressive fashion throughout a wide range of plasma osmolality and that the osmolar threshold for thirst onset is similar to the theoretical osmolar threshold for vasopressin release. The results are compatible with the concept of either a single osmoreceptor subserving both thirst and vasopressin release, or two osmoreceptors sharing similar functional characteristics.

Adult↗

PubMed1989

Effect of vasopressin on bronchial reactivity to histamine.

1. Recent evidence suggests that a high salt diet increases bronchial reactivity, but the underlying mechanism is unclear. 2. To determine whether alterations in circulating vasopressin might be responsible, we have studied the effect of an infusion of vasopressin on the airways of six normal and eight asthmatic subjects measuring the response as expiratory flow at 30% of vital capacity (V30P) in the normal subjects and as forced expiratory volume in 1s (FEV1) in the asthmatic subjects, in a double-blind, placebo-controlled, cross-over study. 3. Vasopressin, given as an infusion at a rate of 2 i.u./h for 1 h, followed by 4 i.u./h for a further hour, produced plasma concentrations of 12.8 and 17 ng/l, respectively, compared with 2.0 and 2.0 ng/l on placebo. 4. Airway reactivity to histamine was measured after 1 and 2 h as the provocative doses of histamine causing a 40% reduction in V30P (PD40V30P) in the normal subjects and a 20% reduction in FEV1 (PD20FEV1) in the asthmatic subjects. 5. There was a small increase in PD40V30P after both vasopressin and placebo in normal subjects (refractoriness) but no change in PD20FEV1 in the asthmatic subjects. 6. There was no significant difference between vasopressin and placebo in V30P or PD40V30P over the 2 h after the drug in the normal subjects or in FEV1 or PD20FEV1 over the 2 h after the drug in the asthmatic subjects. 7. We conclude that alterations in circulating vasopressin are unlikely to be responsible for the increase in bronchial reactivity when dietary salt intake is increased.

Adolescent↗

PubMed1990

Arginine vasopressin release from human platelets after irreversible aggregation.

1. The release of arginine vasopressin from human platelets was investigated in platelet-rich plasma after irreversible aggregation induced by adenosine 5'-pyrophosphate, collagen, sodium arachidonate, thrombin and adrenaline in vitro. 2. Arginine vasopressin levels were significantly higher in the supernatant from stimulated platelet-rich plasma than from unstimulated samples, reaching 3.5 X 10(-12) (range 1.6-12.5 X 10(-12) mol/l in the absence of an aggregating agent, 8.8 X 10(-12) (range 4.2-17.5 X 10(-12) mol/l after adenosine 5'-pyrophosphate, 13.7 X 10(-12) (2.2-63.2 X 10(-12) mol/l after collagen, 7.8 X 10(-12) (2.2-14.6 X 10(-12) mol/l after sodium arachidonate, 7.8 X 10(-12) (2.2-16.3 X 10(-12) mol/l after thrombin and 12.2 X 10(-12) (4.8-32.1 X 10(-12) mol/l after adrenaline. 3. An arginine vasopressin level of 18 X 10(12) mol/l, which can be achieved physiologically, increased the sensitivity of platelets to adenosine 5'-pyrophosphate and collagen in vitro; the same concentration of arginine vasopressin caused a potentiation of the effect of catecholamines on the response of platelets to sodium arachidonate. 4. These results indicate that intraplatelet arginine vasopressin is released during aggregation and suggest that a local release of arginine vasopressin could occur after complete platelet aggregation in vivo.

Adenosine Diphosphate↗

PubMed1992

Vasopressin and angiotensin II in the conscious dog: synergistic effects on renal excretory parameters?

1. The renal effects of angiotensin II were investigated (a) with and without acute blockade of the effects of aldosterone and (b) with and without concomitant infusion of vasopressin. Angiotensin II (2 ng min-1 kg-1) and/or vasopressin (5 pg min-1 kg-1) was infused intravenously into conscious water-diuretic dogs and the effects were quantified by measurements of renal excretion of water, Na+ and K+, as well as determination of plasma renin activity and plasma levels of atrial natriuretic peptide and catecholamines. 2. Angiotensin II alone increased blood pressure by 7% (P < 0.05), decreased effective renal blood flow markedly and reduced urine flow and osmolar and free water clearances. Na+ and K+ excretion did not change significantly. Aldosterone blockade with canrenoate increased Na+ excretion by a factor of 10; subsequent infusion of angiotensin II decreased Na+ excretion by about 50%, the other renal effects being qualitatively similar to those seen without blockade. As expected, vasopressin also decreased diuresis and free water clearance substantially; however, the effect of combined infusion of angiotensin II and vasopressin was not compatible with the notion of additive effects of the two peptides. 3. Angiotensin II alone or in combination with vasopressin did not change the plasma concentrations of atrial natriuretic peptide, adrenaline, noradrenaline, or dopamine. Vasopressin alone exerted its antidiuretic effect without affecting plasma renin activity, plasma aldosterone concentration or renal excretion of Na+ and K+.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗

PubMed2001

Effect of vasopressin on the input-output properties of rat facial motoneurons.

Vasopressin can directly excite facial motoneurons in young rats and mice. It acts by generating a persistent inward current, which is Na(+)-dependent, tetrodotoxin-insensitive and voltage-gated. This peptide-evoked current is unaffected by Ca(++) or K(+) channel blockade and is modulated by extracellular divalent cations. In the present work, we determined how vasopressin alters the input-output properties of facial motoneurons. Whole-cell recordings were obtained from these neurons in the current clamp mode, in brainstem slices of young rats. Repetitive firing was evoked by injecting depolarizing current pulses. Steady-state frequency-current (f-I) relationships were constructed and the effect of vasopressin on these relationships was studied. We found that vasopressin caused a parallel shift to the left of the cell steady-state f-I relationship. This effect persisted in the presence of blockers of K(+) or Ca(++) channels. The peptide effect was distinct from that brought about by Ca(++) channel suppression or by apamin, a blocker of the mAHP. These latter manipulations resulted in an increase in the slope of the steady-state f-I relationship. We conclude that the vasopressin-induced modification of the input-output properties of facial motoneurons is probably exclusively caused by the sodium-dependent, voltage-modulated inward current elicited by the peptide, rather than being due to indirect effects of the peptide on Ca(++) channels, K(+) channels or Ca(++)-dependent K(+) channels. Computer simulation, based on a simple model of facial motoneurons, indicates that the introduction of a conductance having the properties of the vasopressin-dependent conductance can entirely account for the observed peptide-induced shift of the f-I relationship.

Algorithms↗