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)

Tumors from patients with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) have been found to contain large amounts of the antidiuretic hormone vasopressin. A lung tumor from a patient with hyponatremia most likely due to SIADH was removed at surgery and found to contain 23.5 mU vasopressin/g wet weight by radioimmunoassay Slices of this tumor were incubated with phenylalanine-(3)H. Arginine vasopressin-(3)H was purified from the incubate by Sephadex G-25 column chromatography in two different systems, performic acid oxidation, and gradient elution column chromatography with diethylaminoethyl Sephadex. As oxidation of vasopressin results in drastic conformational change with breaking of the ring of the cyclic polypeptide and addition of two cysteic acid residues per molecule, the radioactive material which eluted coincident with vasopressin both before and after this procedure was considered to be arginine vasopressin-(3)H. To our knowledge this is the first demonstration of in vitro biosynthesis of vasopressin by a tumor from a patient with SIADH.Ultrastructurally, the bronchogenic carcinoma was composed of small undifferentiated and granulated cells. The granulated neoplastic cells had well developed organelles (endoplasmic reticulum, free ribosomes) concerned with protein synthesis. Secretion granules present in the tumor cells were small, surrounded by a limiting membrane, and resembled those reported in polypeptide hormone-secreting cells.
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PMID:Biosynthesis of vasopressin in vitro and ultrastructure of a bronchogenic carcinoma. Patient with the syndrome of inappropriate secretion of antidiuretic hormone. 500 44

The effects of several neuropeptides were evaluated using a non-human primate model of age-related memory impairments. Several doses of ACTH4-10, lysine vasopressin, arginine vasopressin, oxytocin and somatostatin were each tested in several aged monkeys. Because data from a large number of non-drug control sessions was collected before, during and after this study, it was possible to define the normal range of control performance for each monkey and statistically determine whether a change in performance under any single dose of drug reflected a significant change from the particular monkey's normal baseline performance. Although none of the neuropeptides produced consistent group effects, evaluations of individual subjects against their own baseline performance revealed reliable changes at certain doses. Arginine vasopressin appeared to produce the best overall effects with three of the five monkeys exhibiting reliable changes in performance from baseline. These same three monkeys also responded positively to the lysine form. Oxytocin impaired memory in three of the six aged monkeys tested over a wide range of doses. Three of six aged monkeys performed better under ACTH4-10 compared to baseline; however, in two of these cases only a single dose was effective. The performance of only one subject was improved under somatostatin, and this was at a single dose only. The data reported here provide evidence for neuropeptides producing behavioral improvement in non-human primates using an appetitive task, eliminating a popular criticism that the data in this literature has depended too heavily on the testing of rodents in shock-motivated tasks. Additionally, the improvements observed in this study involve a behavior that it naturally impaired by age and one which has many operational similarities and some empirical relevance to measures of recent memory in humans. However, these positive findings must be tempered by the lack of robust effects and high individual variation observed.
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PMID:Neuropeptide effects on memory in aged monkeys. 612 93

Hepatocytes incubated with 25 muM [3H] taurocholate rapidly deplete the extracellular medium of [3H] taurocholate and achieve a steady-state level of intracellular bile salt within 15 min. Exposure of cells at steady state with extracellular taurocholate to the catecholamines norepinephrine or epinephrine results in release of 3H from the cells into the incubation medium; the 3H released represents almost exclusively unmetabolized [3H] taurocholate. The hierarchy of effectiveness of the catecholamines, norepinephrine congruent to epinephrine greater than phenylephrine much greater than isoproterenol, is indicative of an alpha-adrenergic mechanism. Induction of [3H] taurocholate release by norepinephrine is inhibited by the alpha-antagonists phenoxybenzamine and phentolamine and by chlorpromazine, but is not affected by the beta-antagonist propranolol, further supporting an alpha-adrenergic basis for this phenomenon. Arginine vasopressin, at concentrations of 1 X 10(-9) M and greater, also induces bile salt release. Classical alpha- and beta-antagonists have minimal effects on vasopressin induced bile salt release. While the peptide hormones angiotensin and oxytocin are, alone, relatively ineffective inducers of bile salt release, oxytocin potentiates the induction of bile salt release by vasopressin, suggesting complex interactions with membrane receptor function. Further studies assessing the interaction of sympathetic neurotransmitters and peptide hormones with bile salt transport and release in the hepatocyte may provide insight into the regulation of hepatic secretory function in the intact animal.
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PMID:Induction of taurocholate release from isolated rat hepatocytes in suspension by alpha-adrenergic agents and vasopressin: implications for control of bile salt secretion. 614 55

This study examined the role of arginine vasopressin in the pressor response to vagal cold block and evaluated a possible interaction between vasopressin and the sympathetic nervous system during vagal block in conscious dogs with (carotid sinus intact) and without (sinoaortic denervated) functional arterial baroreflexes. In both carotid sinus intact and sinoaortic denervated dogs, elimination of the arginine vasopressin pressor system by the specific vasopressin antagonist d(CH2)5Tyr(Me)AVP did not alter the response to vagal block, as evaluated by changes in arterial pressure. Subsequent removal of the sympathetic nervous system by ganglionic blockade abolished the response to vagal block. When ganglionic blockade was induced in the absence of the vasopressin antagonist, the pressor response to vagal block was reduced by only 60%. Arginine vasopressin antagonist after ganglionic blockade reduced the response to vagal block by an amount equivalent to 45% of the original increase in pressure. The effects of blockade of either vasopressin or the sympathetic nervous system on the pressor response to vagal block were significantly greater when the other system had previously been eliminated. Data suggest that both arginine vasopressin and the sympathetic nervous system contribute to the pressor response to vagal block. One interpretation of these results is that vasopressin also interacts centrally to inhibit sympathetic outflow and thus modulates the hemodynamic manifestation of interruption of vagal afferents.
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PMID:The role of vasopressin and the sympathetic nervous system in the cardiovascular response to vagal cold block in the conscious dog. 614 58

Arginine vasopressin (AVP), phenylephrine, and noradrenaline were infused intravenously into conscious and unrestrained adult spontaneously hypertensive (SH) rats and the changes in arterial pressure and heart rate were compared to those in Wistar--Kyoto (WKY) rats. The curve expressing the relationship of the increase in arterial pressure to the logarithm of the plasma concentration of AVP for SH rats was shifted to the left of that for WKY rats by a factor of four. In contrast, the dose--response (arterial pressure) curves for phenylephrine and noradrenaline in SH rats were displaced slightly to the right. In WKY rats, heart rate fell more for a given elevation of arterial pressure during infusions of AVP than during infusions of phenylephrine and noradrenaline; in SH rats, the heart rate response were less pronounced than in WKY rats, and the responses to vasopressin, phenylephrine, and noradrenaline were similar. The results are consistent with the interpretation that cardiovascular reflex activity is particularly enhanced during infusions of AVP in normotensive rats. The absence of this phenomenon in SH rats appears to contribute to the enhanced pressor activity of AVP in these rats.
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PMID:Pressor responsiveness and cardiovascular reflex activity in spontaneously hypertensive and normotensive rates during vasopressin infusion. 616 62

The renal response to arginine vasopressin was investigated with and without the simultaneous administration of the kallikrein inhibitor, aprotinin, in conscious Brattleboro homozygous rats with hereditary diabetes insipidus. Arginine vasopressin caused a marked antidiuretic response (urinary osmolality increased from 118 to 739 mosmol/l) which was accompanied by a significant increase in urinary prostaglandin excretion (prostaglandin E2 and F2 alpha excretion increased by 182 and 441%, respectively). Kallikrein excretion remained unchanged after arginine vasopressin infusion. The infusion of aprotinin diminished urinary kallikrein activity to undetectable levels, decreased potassium excretion significantly and caused a slight fall in urinary prostaglandin excretion. However, aprotinin failed to modify the arginine vasopressin-induced enhancement in prostaglandin excretion (prostaglandin E2 and F2 alpha excretion increased by 168 and 442%, respectively), and the antidiuretic response was also similar to that observed under control conditions. These results indicate that the kallikrein-kinin system is not involved in the renal response to vasopressin in the Brattleboro rat.
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PMID:Effect of aprotinin on the renal response to vasopressin in diabetes insipidus rats. 619 69

Using a newly developed radioimmunoassay to determine the beta-endorphin-like immunoreactivity (beta-EI) in unextracted plasma, the effect of vasopressin injections on plasma beta-EI was investigated in conscious rats. Arginine vasopressin caused a dose-dependent increase of plasma beta-EI from 34.5 to 7.8 fmol ml--1 (n = 6) in vehicle-treated animals to 205.0 +/- 36.1 fmol ml--1 (n = 7) after injection of the highest vasopressin dose employed (486 ng/100 g b.w.). In view of the appreciable cross-reactivity of beta-lipotropin (beta-LPH) in the radioimmunoassay used, plasma was extracted and subjected to gel chromatography on a Sephadex G-50 column. On average, about 70% of the beta-EI co-eluted with human beta-LPH and about 30% with human beta-endorphin in plasma extracts obtained from both control and vasopressin-treated rats. No peripheral conversion of human beta-LPH occurred under the experimental conditions, since after i.v. bolus injection of human beta-LPH 97% of the beta-EI comigrated with human beta-LPH during gel filtration. A similar blood pressure increase to that induced by the vasopressin injections, when elicited by noradrenaline or angiotensin II i.v., was not followed by an elevation of plasma beta-EI. These data indicate that vasopressin stimulates beta-lipotropin and beta-endorphin release into the systemic circulation in vivo.
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PMID:Vasopressin stimulates release of beta-lipotropin and beta-endorphin in conscious rats as measured by radioimmunoassay of unextracted plasma. 626 98

The influence of different neuropituitary hormones on the contraction of the Brazilian opossum uterus in vitro was studied in spayed adults injected with (i) peanut oil (ii) estrogen or (iii) estrogen plus progesterone, and in a fourth group of lactating animals. Two parameters were analyzed from the dose-response curve: pD2 and the relative contractile response compared to the maximal one induced by oxytocin. When oxytocin was administered to the bath, neither pD2 nor the contractile force was affected by any hormonal treatment or lactation. Oxytocin, however, remained in any hormonal status, the most powerful agonist to induce uterine contraction. Lysine vasopressin was the weaker agonist in any hormonal status. It binds slightly less to the isolated uterus than to the hormone-treated one. The maximal contractile force remains unchanged when the uterus is from ovariectomized or steroid-treated animals. However, after lysine vasopressin, uterus from lactating opossum develops a less intense contractility than that observed in other groups. Arginine vasopressin induces a contractile force comparable to that induced by oxytocin in any hormonal status. The affinity of this peptide for the uterine receptor is significantly lower in ovariectomized and estrogen-treated animals; after progesterone injection or in lactating animals the receptor affinity for this hormone is increased to the level of the affinity for oxytocin. Receptor affinity for arginine vasotocin is reduced in any hormonal state and brought to a level comparable to that for oxytocin only in lactating animals. On the other hand, progesterone reduced the maximal contractile force induced by this neuropeptide.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of estrogen and progesterone on the uterine sensitivity in vitro to neuropituitary hormones in the Brazilian marsupial Didelphis albiventris: comparison with lactating animals. 632 93

Vasopressin analogs, which markedly differed in the ratio of pressor versus antidiuretic activity and also in ACTH/beta-endorphin-releasing activity, were used in the present study. The ability of vasopressin and these analogs to enhance the release of adrenocorticotropin-(ACTH-IR) and beta-endorphin-like immunoreactivity (beta-EI) induced by synthetic ovine corticotropin-releasing factor -CRF-(1-41)- was studied in vitro using incubated rat anterior pituitary quarters. Arginine vasopressin (AVP) potentiated the action of CRF-(1-41) 2- to 4-fold. Vasopressin analogs, which possess direct CRF-like activity when given alone, also enhanced beta-EI release caused by CRF-(1-41); the lowest concentration able to potentiate CRF-(1-41) activity was closely correlated with the ED50 value of these analogs for direct CRF-like activity. The vasopressin analog 1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid)-2-(O-methyl)tyrosine-8-arginine-vasopressin blocked the release of ACTH-IR induced by AVP; however, this analog failed to prevent the potentiation by AVP of ACTH-IR release caused by CRF-(1-41), but enhanced itself the action of CRF-(1-41). Two analogs, which exhibited no direct CRF-like activity and which also did not antagonize the CRF-like activity of AVP, markedly enhanced the ACTH-IR and beta-EI response to CRF-(1-41).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Stimulation of adrenocorticotropin/beta-endorphin release by synthetic ovine corticotropin-releasing factor in vitro. Enhancement by various vasopressin analogs. 632 45

These studies tested the effects of isoproterenol on potassium secretion in the isolated perfused cortical collecting tubule. Isoproterenol, 10(-6) M (n = 6) and 10(-4) M (n = 2), added to bathing solution produced a significant fall in potassium secretion [13.5 +/- 1.2 to 8.0 +/- 0.9 peq X mm-1 X min-1 (P less than 0.01)] and in transepithelial voltage (P less than 0.01) compared with time controls (n = 9). Pretreatment with propranolol abolished this effect (n = 4). Addition of propranolol alone to the bath caused no significant change in potassium secretion (n = 8). 8-[p-Chlorophenylthio]cAMP (10(-4) M, isotonic perfusate) added to the bath produced a significant fall in potassium secretion [11.5 +/- 1.7 to 7.2 +/- 1.3 peq X mm-1 X min-1, n = 7 (P less than 0.01)]. Arginine vasopressin (25 microU/ml), which also stimulates adenylate cyclase activity in this segment, had no significant effect on potassium secretion (n = 10). When chloride was replaced by methyl sulfate in all solutions (n = 6), there was a significant attenuation in the fall in potassium secretion in experiments with 10(-6) M isoproterenol compared with experiments with chloride-containing bath solutions (P less than 0.05). These data suggest that isoproterenol has a specific action of reducing potassium secretion in the cortical collecting tubule either through alternating chloride transport per se or through some other effect dependent on the presence of chloride (e.g., hydrogen ion secretion). Also, this effect is probably mediated by cAMP-dependent events. The lack of effect of vasopressin on potassium secretion suggests that separate cells or cellular pools of cAMP are involved in hormonal stimulation by isoproterenol and vasopressin in this nephron segment.
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PMID:Effects of isoproterenol on potassium secretion by the cortical collecting tubule. 633 Nov 72


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