Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anesthesia in rats produced by urethane administered intraperitoneally caused (1) peritoneal fluid accumulation; (2) inability to undergo a renal response to NaCl or water loading, and (3) pronounced hyperosmolality of body fluids without affecting plasma [Na+]. The impairment of the renal function appears not to be due to anesthesia per se, angiotensin, aldosterone, vasopressin or renal nerves. It probably is attributable to osmotoxicity of the mesenteric vasculature. By contrast, urethane administered intravenously evokes a brisk osmotic diuresis without fluid leakage into the peritoneum. Plasma osmolality is still increased. The osmotic toxicity to the mesenteric vasculature, poor renal function and altered composition of body fluids that occur after intraperitoneal urethane may complicate the interpretation of data obtained in rats anesthetized in this manner.
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PMID:Urethane anesthesia in rats. Altered ability to regulate hydration. 702 89

Osmoreceptor sensitivity, as estimated by the plasma vasopressin (AVP) response to hypertonic saline infusion, increases with age. We studied volume-pressure sensitivity, as estimated by the plasma AVP response to orthostasis, in healthy young (19-31 yr old; n = 12) and old (62-80 yr old; n = 15) subjects. After remaining recumbent overnight (minimum of 8 h), subjects stood quietly for 8 min. Cardiovascular changes on standing were not influenced by age. The peak plasma AVP response was greater in the young than in the old (P = 0.02, by rank sum test). When categorized as responders (peak AVP response, greater than or equal to 3 pg/ml) or nonresponders (peak response, less than 3 pg/ml), the young group included 11 responders and 1 nonresponder, while the old group included 8 responders and 7 nonresponders (P = 0.03, by Fisher exact test). There was no difference in the marked increase in plasma norepinephrine on standing between old responders (n = 6) and old nonresponders (n = 4). These studies indicate that failure to release AVP in response to orthostasis is more common in the elderly than in the young. The intact norepinephrine response to orthostatis in the elderly, regardless of the AVP response, suggests that the age-related defect is distal to the vasomotor center in the afferent limb of the baroreceptor reflex arc. Insensitivity to the volume and pressure changes accompanying hypertonic saline infusion may contribute to the previously noted augmented AVP response of the elderly to hyperosmolality.
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PMID:Age-related failure of volume-pressure-mediated vasopressin release. 705 50

Seven subjects with Kallmann's syndrome were studied to determine whether they had disturbances of fluid homeostasis. Simultaneous measurements of urine and plasma osmolality (Uosm and Posm, respectively) were made during free access to fluids. The Uosm-Posm relationship was abnormal in five patients on at least one occasion. Patient 2 was frequently overhydrated (Posm less than or equal to 280 mosmol/kg) and patient 5 excreted a dilute urine when his Posm was 290 mosmol/kg. The three subjects (1, 5, and 7) tending to have an increased Psom (greater than or equal to 300 mosmol/kg) were able to concentrate their urine (Uosm greater than 800 mosmol/kg) and denied polyuria and polydipsia. Their elevated Posms could be explained by impairment of thirst, rather than increased excretion of water, because the patients concentrated their urines at normal Posms during fluid deprivation. The osmotic threshold for vasopressin release was decreased (Posm = 270.6 mosmol/kg) in one patient and increased (Posm greater than or equal to 295 mosmol/kg) in two others of the seven patients. The elevated osmotic threshold was not due to chronic hyperosmolality or a generalized defect in vasopressin secretion. In the patient with the highest osmotic threshold (Posm = 296 mosmol/kg) and Posms between 289--301 mosmol/kg during free access to fluid, the osmotic threshold decreased to only 293 mosmol/kg after 6 weeks of adequate hydration and desmopressin acetate. However, in response to hypotension induced by trimethaphan, he increased his plasma vasopressin from 1--26 microU/ml. In conclusion, some patients with Kallmann's syndrome may have osmoreceptor dysfunction and abnormal thirst regulation, indicating more extensive hypothalamic involvement than previously appreciated.
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PMID:Altered osmotic threshold for vasopressin release and impaired thirst sensation: additional abnormalities in Kallmann's syndrome. 710 21

To evaluate a central role of angiotensin in vasopressin (ADH) release in response to hyperosmolality or hypovolaemia, we examined in conscious rats the effects of intraperitoneal (ip) injections of 2 ml/100 g body weight of hypertonic saline or polyethylene glycol (PEG; 250 mg/ml of 145 mM NaCl) on plasma ADH and angiotensin II (AII) levels and of intracerebroventricular (icv) administrations of Sar1-Ala8-AII (a competitive receptor blocker for AII) on the plasma ADH responses to the ip injections. Thirty min after ip injections of 900 mM NaCl, plasma ADH, osmolality and sodium increased with unchanged plasma AII and with reduced haematocrit. Two h after ip administrations of PEG, plasma ADH, AII and haematocrit were augmented with unaltered plasma osmolality and sodium. The responses of plasma ADH to ip injections of 900 mM NaCl and PEG were significantly inhibited (P less than 0.05) by 1 microgram of Sar1-Ala8-AII injected icv 5 min before blood samplings which had no appreciable effect on plasma osmolality, electrolytes and haematocrit. Based on these results, we concluded that angiotensin may participate in both the hyperosmolality- and hypovolaemia-induced ADH secretion by acting on the central nervous system.
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PMID:Central role of angiotensin in the hyperosmolality- and hypovolaemia-induced vasopressin release in conscious rats. 715 28

We investigated the regulation of cellular prostaglandin E2 (PGE2) biosynthesis in rabbit renomedullary interstitial cells in tissue culture. Arachidonic acid markedly stimulated PGE2 biosynthesis by these cells. Repeated exposure to arachidonic acid, resulted in progressively less stimulation of PGE2 biosynthesis. Potassium and dexamethasone diminished PGE2 biosynthesis by decreasing the rate of arachidonic acid release from the endogenous arachidonic acid storage pool. Hyperosmolality, like angiotensin II, bradykinin, and arginine vasopressin, stimulated PGE2 biosynthesis by increasing the rate of arachidonic acid release. Inhibitors of protein synthesis diminished angiotensin II-, bradykinin-, and arginine-vasopressin-stimulated PGE2 biosynthesis by decreasing hormone-stimulated arachidonic acid release. The effects of potassium, dexamethasone, arachidonic acid, and hyperosmolality on PGE2 biosynthesis were unaffected by protein synthesis inhibitors. Hormone-stimulated phospholipase activation is dependent on protein synthesis, whereas potassium, hyperosmolality, and dexamethasone alter the release of arachidonic acid from cellular lipids via a mechanism that is independent of protein synthesis.
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PMID:Regulation of prostaglandin E2 synthesis by angiotensin II, potassium, osmolality, and dexamethasone. 740 48

An adolescent boy with essential hypernatremia, absent corpus callosum, mental retardation, hypodipsia, and partial diabetes insipidus with "inappropriate" ADH regulation and secretion was studied regarding factors controlling ADH and neurophysin release. Persistent hyperosmolality was noted while on 100 mEq sodium intake daily. Endogenous vasopressin activity was demonstrated after prolonged water deprivation. Hypertonic saline infusion produced increased volumes but dilute urine. Aqueous pitressin increased urinary osmolality, decreased serum osmolality, urine flow rate, and free water clearance. Stable water diuresis was induced by water loading and on normal saline infusion. Nicotine-stimulated neurophysin remained unexpectedly low and below the level of detectability when sampled during the physiologic studies, whereas oestrogen-stimulated neurophysin was elevated during oestrogen stimulation, water loading, and orthostasis procedures. Plasma vasopressin was suppressed with water loading but remained suppressed 90 min after tilt table testing. These data indicate impairment of the osmoreceptor mechanism: however, since the patient had a normal response of oestrogen-stimulated neurophysin, that part of the neurohypophysis appears intact. Chlorpropamide was effective in alleviating the hyperosmolar state acutely and maintained normal osmolar concentrations during two years of therapy.
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PMID:Essential hypernatraemia, antidiuretic hormone and neurophysin secretion: response to chlorpropamide. 746

1. During pregnancy in most species, the resting levels of plasma angiotensin II, plasma ACTH (corticotropin) are increased. The concentration of vasopressin is also increased relatively to the osmolality in rats and in humans. 2. In the pregnant state mean arterial pressure is decreased, despite an increase in blood volume. Vasopressin and ACTH responses to hypotension are altered in pregnant ewes; the relationship between mean arterial pressure and vasopressin or ACTH response is shifted to the left, consistent with a change in set-point for regulation of mean arterial pressure. The vasopressin and cortisol responses to hypotensive haemorrhage are also altered in the pregnant dog; in this case the slope of the relation between mean arterial pressure and hormone response is decreased. 3. The decrease in hormone responses to hypotension is stimulus-specific; ACTH responses to hypoglycaemia are increased in the pregnant ewe and AVP responses to hyperosmolality are not altered in the pregnant ewe. 4. The heart rate responses to hypotension are also decreased in pregnant ewes, consistent with the observation that baroreflex responses are decreased in the pregnant rat. 5. The data suggest that a change in regulation of arterial pressure alters the hormonal responses to hypotension in the pregnant state.
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PMID:Reflex regulation of hormonal responses during pregnancy. 762 8

The physiology of the release of antidiuretic hormone (ADH) from the posterior pituitary is briefly reviewed. The importance of both osmolar and non-osmolar stimuli is emphasised. Osmolar and non-osmolar factors usually reinforce each other; for example, hydropenia leads to hyperosmolality and hypovolaemia, both promoting ADH release, while hydration has the opposite effect. In disease, osmolar and non-osmolar factors may become dissociated leading to baroreceptor-mediated ADH release in the presence of hyponatraemia and hypo-osmolality. Examples include heart failure, glucocorticoid or thyroxine deficiency, hepatic cirrhosis and nephrotic syndrome with or without the superimposed effect of diuretics, i.e. conditions in which circulatory, and in particular effective arterial, volume is reduced. It is dangerous to label such conditions as 'inappropriate' secretion of ADH since the maintenance of circulating volume is at least as important a physiological requirement as the defence of tonicity. The syndrome of inappropriate secretion of ADH (SIADH) is uncommon in childhood and should only be diagnosed when physiological release of ADH in response to non-osmolar as well as osmolar factors has been excluded. Criteria for the correct identification of SIADH are discussed; the presence of continuing urinary sodium excretion in the presence of hyponatraemia and hypo-osmolality is essential to the diagnosis. SIADH in children is usually due to intracranial disease or injury. The mainstay of treatment is water restriction which reverses all the physiological abnormalities of the condition. Hypertonic saline is rarely indicated for the short-term control of neurological manifestations such as seizures. Drugs have little or no place in the treatment of SIADH in children.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The syndrome of inappropriate secretion of antidiuretic hormone. 861 39

1. To investigate the mechanism of hepatic V1a vasopressin receptor down-regulation in streptozotocin-induced diabetes mellitus in the rat, we measured hepatic V1a receptor mRNA by in situ hybridization histochemistry using oligonucleotide probes to the V1a receptor and Northern blotting. 2. Diabetes mellitus caused hyperglycaemia, hyperosmolality and increased plasma vasopressin concentrations (P < 0.01). Hepatocyte V1a receptor mRNA was reduced by 76% in diabetic rats (P < 0.01) and by 53% in insulin-treated diabetic rats (P < 0.01) versus control rats, in parallel with reduced V1a radioligand binding and vasopressin-stimulated inositol phosphates production. There was a similar decrease in hepatic V1a/18S mRNA density ratio in the diabetic and diabetic+insulin groups (both P < 0.05 versus control). 3. These findings suggest that altered V1a mRNA transcription is responsible for the reduced hepatic V1a receptor density in diabetes mellitus.
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PMID:Down-regulation of vasopressin V1a receptor mRNA in diabetes mellitus in the rat. 763 50

In the rat medullary thick ascending limb (MTAL), hyperosmolality inhibits transepithelial HCO3- absorption (JHCO3-) by inhibiting apical membrane Na+/H+ exchange. To examine signaling mechanisms involved in this regulatory response, MTALs were isolated and perfused in vitro with 25 mM HCO3- solutions (290 mosmol/kg H2O). Osmolality was increased in lumen and bath solutions by addition of 300 mM mannitol or 75 mM NaCl. Addition of mannitol reduced JHCO3- by 60% and addition of NaCl reduced JHCO3- by 50%. With the protein tyrosine kinase (PTK) inhibitor genistein (7 microM) or herbimycin A (1 microM) in the bath, addition of mannitol reduced JHCO3- only by 11% and addition of NaCl reduced JHCO3- only by 15%. Staurosporine (10(-7) M) or forskolin (10(-6) M) in the bath had no effect on inhibition of JHCO3- by hypertonic NaCl. Genistein had no effect on inhibition of JHCO3- by vasopressin (a cyclic AMP-dependent process) or stimulation of JHCO3- by prostaglandin E2 (a protein kinase C-dependent process). Under isosmotic conditions, addition of genistein or herbimycin A to the bath increased JHCO3- by 30% through stimulation of apical membrane Na+/H+ exchange. Addition of the tyrosine phosphatase inhibitor molybdate (50 microM) to the bath reproduced the inhibition of JHCO3- observed with hyperosmolality. These data indicate that 1) the effect of hyperosmolality to inhibit MTAL HCO3- absorption through inhibition of apical membrane Na+/H+ exchange is mediated via a PTK-dependent pathway that functions independent of regulation by cyclic AMP and protein kinase C, and 2) a constitutive PTK activity inhibits apical membrane Na+/H+ exchange and HCO3- absorption under isosmotic conditions. Our results suggest that tyrosine phosphorylation is a critical step in inhibition of the apical Na+/H+ exchanger isoform NHE-3 by hyperosmolality.
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PMID:Hyperosmolality inhibits bicarbonate absorption in rat medullary thick ascending limb via a protein-tyrosine kinase-dependent pathway. 773 Mar 71


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