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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As a model to study effects of chronic, excessive salt loading on circulation, Pekin ducks were adapted to 2% saline solution as their sole water supply, while fresh-water-adapted animals were used as controls. Due to the development of salt-eliminating glands, salt-adapted ducks are able to cope indefinitely with this salt stress which means a daily ingestion of 5-6 g NaCl per kg body weight per day, associated with a chronic elevation of plasma osmolality and plasma sodium by 5-8% above normal and an up to 3-fold increase of antidiuretic hormone concentration in comparison to animals maintained on fresh water. Salt loading for up to 14 months did neither increase arterial mean, nor diastolic, nor pulse pressure. On the contrary, arterial mean and diastolic pressure were slightly lower in the salt-adapted than in the fresh-water-adapted animals, while pulse pressure and heart rate did not differ. Circulatory adaptation to removal and reinfusion of 10% of the estimated blood volume was identical in salt-water and fresh-water-adapted ducks. It is concluded that even excessive chronic salt loading resulting in chronic hyperosmolality with high plasma levels of sodium and antidiuretic hormone does not alter hemodynamic adaptation, provided that efficient compensating mechanisms are at the animal's disposal.
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PMID:Blood pressure and arginine vasotocin in normonatremic and hypernatremic ducks. 400 22

A patient with the chronic hypernatraemia syndrome is described. Using a sensitive and specific radioimmunoassay, the plasma arginine-vasopressin (AVP) level was measured under various conditions. With an unrestricted diet, the plasma AVP level was inappropriately low for the degree of plasma hyperosmolality (0.9 pmol/l and 302 mOsm/kg, respectively). After chronic water loading, plasma osmolality was 271 mOsm/kg, plasma AVP level 1.5 pmol/l, and the urine remained hypertonic with respect to the plasma. During hypertonic saline infusion, plasma osmolality increased from 271 to 294 mOsm/kg without a concomitant increase in the plasma AVP concentration. After sc injection of apomorphine and after haemodynamic stimulation, the plasma AVP concentration increased from 0.8 to 36 pmol/l and from 1.2 to 6.3 pmol/l, respectively. These data demonstrate a selective deficiency in the osmoregulation of the AVP secretion. The observed neuroendocrine abnormalities may be linked to a congenital malformation of the brain.
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PMID:Regulation of vasopressin secretion in a patient with chronic hypernatraemia. 407 75

A physiological explanation for sustained hyperosmolality was sought in a patient with histiocytosis. During 23 days of observation with only sodium intake regulated at 100 mEq daily, elevation (mean 310 mOsm/kg of water) and fluctuation (range 298-323) of the fasting plasma osmolality were recorded. The presence of endogenous vasopressin was indicated by the patient's ability to concentrate the urine to as high as 710 mOsm/kg of water with a creatinine clearance of 84 cc/min, and by dilution of the urine in response to alcohol. The failure of increasing fluid intake to as high as 6.2 liters daily to lower the plasma osmolality indicated that deficient fluid intake was not solely responsible for the elevated plasma osmolality. Hypertonic saline infusion during water diuresis resulted in the excretion of an increased volume of dilute urine. The water diuresis continued despite a rise in plasma osmolality from 287 to 339. An isotonic saline infusion initiated during hydropenia resulted in a water diuresis which continued despite a rise in the plasma osmolality from 303 to 320. Stable water diuresis induced during recumbency by either oral ingestion of water or intravenous infusion of normal saline was terminated by orthostasis and resumed with the return to the recumbent position. Antecedent alcohol ingestion blocked the antidiuresis of orthostasis. The data are interpreted as indicating impairment of the osmoreceptor mechanism as the primary cause of the hyperosmolar syndrome. They also indicate that vasopressin secretion was regulated primarily by changes in effective blood volume. Chlorpropamide was found to be an effective treatment for the syndrome.
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PMID:"Essential" hypernatremia due to ineffective osmotic and intact volume regulation of vasopressin secretion. 510

Hyperosmolality occurs when there are defects in the two major homeostatic mechanisms required for water balance-thirst and arginine vasopressin (AVP) release. In this situation hypotonic fluids are lost in substantial quantities causing depletion of both intracellular and extracellular fluid compartments. Patients with essential hypernatremia have defective osmotically stimulated AVP release and thirst but may have intact mechanisms for AVP release following hypovolemia. Hyperosmolality can also be seen in circumstances in which impermeable solutes are present in excessive quantities in extracellular fluid. Under these conditions there is cellular dehydration and the serum sodium may actually be reduced by water drawn out of cells along an osmotic gradient. Hyposmolality and hyponatremia may be seen in a variety of clinical conditions. Salt depletion, states in which edema occurs and the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) may all produce severe dilution of body fluids resulting in serious neurologic disturbances. The differential diagnosis of these states is greatly facilitated by careful clinical assessment of extracellular fluid volume and by determination of urine sodium concentration. Treatment of the hyposmolar syndromes is contingent on the pathophysiology of the underlying disorder; hyponatremia due to salt depletion is treated with infusions of isotonic saline whereas mild hyponatremia in cirrhosis and ascites is best treated with water restriction. Severe symptomatic hyponatremia due to SIADH is treated with hypertonic saline therapy, sometimes in association with intravenous administration of furosemide. Less severe, chronic cases may be treated with dichlormethyltetracycline which blocks the action of AVP on the collecting duct.
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PMID:The clinical physiology of water metabolism. Part III: The water depletion (hyperosmolar) and water excess (hyposmolar) syndromes. 624 83

We investigated the effects of hyperosmolality, chronic treatment with lithium chloride (LiCl), and the addition of LiCl in vitro on vasopressin-sensitive (VP) adenylate cyclase (AdC) and cAMP phosphodiesterase (cAMP-PDIE) activities in the medullary thick ascending limb of Henle's loop (MAL) and medullary collecting tubule (MCT) microdissected from the outer medulla of the rat kidney. A hyperosmolar medium (800 mosmol) markedly enhanced AdC activity stimulated by 10(-6) M VP specifically in MCT, while having little effect or slightly decreasing VP-stimulated AdC in MAL, compared to activities under standard isotonic conditions. Hyperosmolality decreased cAMP-PDIE activity to about the same degree in MAL and MCT. Inclusion of LiCl in the incubation medium (15-20 mM) caused a significant dose-dependent inhibition of VP-stimulated AdC activity in both MAL and MCT, but had no effect on CAMP-PDIE in either segment. AdC and cAMP-PDIE activities in MAL and MCT from chronic LiCl-treated polyuric rats did not differ from controls when assayed under standard isotonic conditions. However, when assayed in a hyperosmolar (800 mosmol) medium, VP-sensitive AdC activity was significantly lower (P < 0.01) in MCT from LiCl-treated rats compared to control levels, while VP-sensitive AdC in MAL did not differ in LiCl-treated and control rats. The present results suggest that lowered VP-sensitive AdC activity in MCT of LiCl-treated polyuric rats may contribute to the observed lower concentrating ability and collecting tubule resistance to VP. Inhibition of VP-sensitive AdC in MAL as well as MCT by the acute addition of LiCl in vitro may explain the decreased urinary diluting ability observed with acute infusions of Li salts in vivo in the rat.
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PMID:Lithium-induced polyuria: effect of lithium on adenylate cyclase and adenosine 3',5'-monophosphate phosphodiesterase in medullary ascending limb of Henle's loop and in medullary collecting tubules. 625 74

Osmoregulation was studied in 13 mountaineers who had experienced long-term exposure to high altitude on Mt Everest. Serum osmolality rose from 290 +/- 1 mOsm/kg to 295 +/- 2 mOsm/kg at 5,400 m and finally to 302 +/- 4 mOsm/kg at 6,300 m after a mean of 26.5 days above 5,400 m. Despite this degree of osmoconcentration, plasma arginine-vasopressin concentration remained unchanged: 1.1 +/-0.1 microU/mL at sea level, 0.8 +/- 0.1 microU/mL at 5,400 m, and 0.9 +/- 0.1 microU/mL at 6,300 m. Urinary vasopressin excretion was also similar at all three altitudes. We conclude that prolonged exposure to high altitude may result in persistent impairment of osmoregulation, caused in part by an inappropriate arginine-vasopressin response to hyperosmolality.
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PMID:Impaired osmoregulation at high altitude. Studies on Mt Everest. 642 58

The use of vasopressin to limit the polyuria of the brain-dead organ donor is a controversial subject. It is held that the associated vasoconstriction may result in ischemic damage to transplantable organs. However, the derangements in the intravascular--and thereby interstitial and intracellular--fluid and electrolyte balances associated with diabetes insipidus may lead to gross fluid shifts in the organ donor. Aggressive resuscitation with crystalloid solutions may aggravate these fluid shifts, contribute to the development of interstitial and intracellular edema, and ultimately result in cardiovascular failure and the rejection of the organs for transplantation. Theoretically, a minute amount of vasopressin is required for the maintenance of normal intravascular fluid and electrolyte balance, and it is best administered as a continuous i.v. infusion. We report on our study of an animal model of a brain-dead organ donor, in which polyuria, hypernatremia, and hyperosmolality developed. The administration of low-dose (2-10 microU/kg/min) vasopressin by continuous infusion maintained plasma sodium and osmolality in the normal range over the course of the experiments (24 hr) in the experimental group. Cardiovascular function remained stable in both control and experimental vasopressin-infusion) groups, with the only significant difference being a moderate rise in pulmonary artery pressure. It would appear that early low-dose vasopressin supplementation by continuous i.v. infusion may improve donor management. The maintenance of intravascular homeostasis may contribute to the quality and number of organs for transplantation.
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PMID:Vasopressin supplementation in a porcine model of brain-dead potential organ donors. 649 67

Rats were treated with a single injection of either capsaicin (50 mg kg-1 s.c.) or vehicle on day 2 after birth. When the animals were adult, they were challenged with osmotic (water deprivation) and haemodynamic (acute hypotension) stimuli that normally evoke vasopressin release. Capsaicin-treated and vehicle-injected rats showed similar body weight losses and plasma osmolalities following 48 h of water deprivation. Thus it appears that neonatal treatment with capsaicin does not impair the antidiuretic response to plasma hyperosmolality. Following acute ganglion blockade in the presence of angiotensin converting enzyme inhibition, there was some recovery of blood pressure in the vehicle-injected rats, but recovery was significantly (P less than 0.001) less in the capsaicin-treated animals. The recovery may be attributed to vasopressin since it was abolished by an antagonist selective for the pressor action of the peptide (d(CH2)5DAVP). These results suggest that neonatal treatment with capsaicin impairs vasopressin-mediated recovery of blood pressure following acute hypotension. The possible involvement of baro- or chemoreceptor afferents is discussed.
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PMID:Neonatal capsaicin treatment impairs vasopressin-mediated blood pressure recovery following acute hypotension. 670 93

A 24-year-old female with gastrointestinal disturbances, nausea and vomiting, had a convulsion with loss of urine and bitten lips on the 5th day of hospitalization. A significant decrease of sodium and potassium levels and lowered osmolality of the serum as well as urinary hyperosmolality permitted the diagnosis of the so-called syndrome of inappropriate antidiuretic hormone release (SIADH) of unknown aetiology, described by Schwartz-Bartter. Twice short tests for porphyria were negative; then the elevated porphyrin precursors collected in 24 h urine indicated the existence of an acute intermittent porphyria. A clinical follow-up and improvement were demonstrated by the EEG findings. Since animal experiments and pathohistological findings indicate that porphyrin metabolites such as delta-amino laevulinic acid and porphobilinogen may influence inhibitory and neurosecretory structures in central nervous tissue and interfere with GABA, cerebral hyperexcitability as well as disturbance of electrolytes may be explained. Finally, the question of whether the EEG changes are due to the significant electrolyte disturbances or are typical signs of acute intermittent porphyria is discussed.
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PMID:[EEG changes in a patient with acute intermittent porphyria and a Schwartz-Bartter syndrome (SIADH)]. 681 70

The effects of ablation of the nucleus medianus on drinking and vasopressin secretion were studied in male Long-Evans rats. The amount of water drunk in 1 h was assessed after subcutaneous injection of 5.8% NaCl (13.34 mosm/kg) or of angiotensin II (1.5 mg/kg). In a separate test with no water available, plasma vasopressin was measured 15 min after the above dose hypertonic saline. Ablation of the nucleus medianus, or the dorsal and anterior portions of the nucleus medianus, blocked drinking to hypertonic saline or angiotensin II and attenuated the vasopressin response to hyperosmolality. Animals with septal or diagonal band lesions showed responses comparable to sham-operated rats. These results indicate that a neural pathway important for fluid balance passes through, or terminates in, the nucleus medianus.
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PMID:Deficits in drinking and vasopressin secretion after lesions of the nucleus medianus. 688 60


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