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)

One the basis of two special typical cases, the authors detail the symptoms and signs and consider the physiopathology of inappropriate secretion of antidiuretic hormone related to vincristine. Urinary ADH was measured in both cases. ADH levels could be studied on ten consecutive occasions during the course of one of the cases (obs. n 1). Eleven similar cases have been found in the literature. ADH was measured in only three of them. Methods of treatment are considered, with particular emphasis on the role of demeclocycline.
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PMID:[Inappropriate secretion of antiduiuretic hormone during acute leukaemia treated with vincristine. Two cases (author's transl)]. 11 79

Fourteen patients with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) have been treated with demethylchlortetracycline (demeclocycline) 1200 mg daily. In 12 patients the underlying lesion was malignant. The serum sodium returned to normal (greater than 135 mmol/l) in all patients after a mean of 8.6 days (SD +/- 5.3 days). Blood urea rose significantly from the pretreatment level of 4.2 +/- 2.3 mmol/l to 10.1 +/- 5.1 mmol/l at ten days (P less than 0.001). The average maximum blood urea was 13.4 +/- 6.8 mmol/l. In four patients the urea rose above 20 mmol/l, and in two of these demecyocycline was discontinued because of thie rise. The azotaemia could be attributed to a combination of increased urea producation and a mild specific drug-induced nephrotoxicity. Discontinuation of demeclocycline in six patients led to a fall in serum sodium, in one case precipitously, and return of the urea towards normal levels. Demeclocycline appears therefore to be an effective maintenance treatment of SIADH, and the azotaemia that occurs is reversible and probably dose dependent.
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PMID:Demeclocycline in the treatment of the syndrome of inappropriate secretion of antidiuretic hormone. 11

A 72-year-old woman with the syndrome of inappropriate secretion of antidiuretic hormone of unknown cause during more than one year of observation is reported. Plasma vasopressin levels were excessively elevated, even during a water load test. Her serum electrolyte abnormalities and general state were ameliorated after fluid restriction. During treatment with demeclocycline the patient was able to increase fluid without deterioration.
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PMID:The syndrome of inappropriate secretion of antidiuretic hormone. A case report. 11 86

Intraarterial vasopressin infusions were given to 46 patients with pyloroduodenal hemorrhage. Hemorrhage was angiographically and clinically controlled in 15 patients, with recurrent bleeding in five. Bleeding was not controlled in 31 patients; seven of these underwent Gelfoam embolization, with bleeding controlled in three. It is concluded that intraarterial vasopressin infusions are not as effective in controlling pyloroduodenal hemorrhage as in other areas of the gastrointestinal tract.
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PMID:Pyloroduodenal bleeding and intraarterial vasopressin: clinical results. 11 8

In the urinary bladder of amphibia, hypertonicity of the serosal bath (SH) evokes an increase in transepithelial water permeability, the characteristics of which resemble the response to antidiuretic hormone (ADH). The ionic dependency, in particular for Ca2+, appears very similar for SH- and ADH-induced water fluxes. In the present experiments La3+ was used as a probe to study the Ca2+-dependency of the hydrosmotic response to SH in isolated urinary bladder of the toad Bufo marinus. Addition of La3+ (5 mM) on the serosal side of the membrane produced a significant and reversible increase in basal transepithelial water flux. The hydrosmotic response elicited by adding 250 mM mannitol to the serosal Ringer's solution was inhibited by 30% in the absence of serosal Ca2+. Similarly, the hydrosmotic response to SH was inhibited by 37%, 30% and 40% when 5 mM La3+ was added to the serosal medium 30 min before, concommitantly with, or 60 min after induction of SH. The inhibition of transepithelial water flux observed in the absence of serosal Ca2+ or in the presence of serosal La3+ was reversible. The results support a critical role for Ca2+ in the modulation of transepithelial water permeability in the urinary bladder of amphibia. Ca2+ presumably exerts its effects at a post-cyclic AMP step.
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PMID:Reversible inhibition by lanthanum of the hydrosmotic response to serosal hypertonicity in toad urinary bladder. 11 63

Mesenteric vascular effects of prostaglandins B2 and F2 alpha were studied and compared to those of vasopressin in the dog, cat and baboon. Vasopressin reduced superior mesenteric blood flow (SMBF) 80-100%, and significantly increased hepatic arterial blood flow and systemic arterial pressure. Prostaglandin B2 produced vasodilatation at low doses and biphasic vasodilatation/vasoconstriction at high doses. Prostaglandin F2 alpha elicited only vasoconstriction, reducing SMBF, left gastric, and inferior mesenteric blood flow 80-100%. Systemic arterial pressure was not significantly changed. Thus, vasopressin and prostaglandin F2 alpha are equally effective mesenteric vasoconstrictors. Because of reduced systemic effects, prostaglandin F2 alpha has excellent potential as a mesenteric vasoconstrictor to control gastrointestinal hemorrhage.
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PMID:Mesenteric vascular effects of prostaglandins F2 alpha and B2. Possible advantages over vasopressin in control of gastrointestinal bleeding. 11 58

The effects of a number of peptides which are found in the gastrointestinal tract have been ascertained on the direct current recorded dorsal and ventral root responses of the isolated hemisected toad spinal cord. Motilin, substance P, bombesin, neurotensin, and thyrotropin releasing hormone had potent depolarizing actions on dorsal root terminals and motoneurons. These substances evoked discernable effects at concentrations as low as 10--7 M, or even lower with motilin. The effects of motilin, neurotensin, and thyrotropin-releasing hormone were greatly reduced or abolished by perfusion of the preparation with tetrodotoxin. Adrenocorticotrophic hormone, secretin, and pancreozymin (cholecystokinin) also depolarized dorsal root terminals and motoneurons. The effects of secretin and cholecystokinin were not abolished by tetrodotoxin. Leu- and Met-enkephalin had weak hyperpolarizing actions on the dorsal and ventral root potentials of repetitively stimulated preparations. Gastrin, gastric inhibitory peptide, glucagon, and somatostatin had no apparent effects on the responses of the preparation. Angiotensin and vasopressin both had rather weak depolarizing effects on the dorsal and ventral roots.
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PMID:Actions of various gastrointestinal peptides on the isolated amphibian spinal cord. 11 60

An enzyme which catalyzes the deamidation of thyroliberin (TRF; less than Glu-His-Pro-NH2) has been purified 110-fold from extracts of bovine anterior pituitary by ammonium sulfate fractionation, ion exchange chromatography on DEAE-cellulose, and gel filtration. This enzyme of 76,000 molecular weight (as estimated by gel filtration) exhibits maximal activity at neutral pH (optimum pH 7.4 to 7.6) in buffers of high ionic strength supplemented with thiol-protecting agents. As indicated by the strong inhibition of the enzymatic activity by N-ethylmaleimide and Hg2+, as well as by the extreme sensitivity toward diisopropyl fluorophosphate, -SH, and -OH residues apparently represent essential functional groups of the enzyme. The stereospecific deamidation of TRF (Km = 4.1 . 10(-4) M) is inhibited competitively by TRF analogues which contain proline or by the proline containing biologically active peptides luliberin (LH-RF), oxytocin, vasopressin, angiotensin II, and Substance P. TRF analogues without proline or peptide amides without proline are ineffective. This enzyme cleaves the appropriate Pro-X bonds in luliberin, angiotensin II, pyroGlu-His-Pro-Gly-NH2, and the collagenase substrate Z-Gly-Pro-Leu-Gly-Pro. Thus, it may be characterized as a post-proline-cleaving enzyme.
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PMID:Characterization of "thyroliberin-deamidating enzyme" as a post-proline-cleaving enzyme. Partial purification and enzyme-chemical analysis of the enzyme from anterior pituitary tissue. 11 64

The polyuria and hyposthenuria noted particularly following blood transfusion after prolonged periods of hypotension (dog, monkey) seem best explained by a prostaglandin-antidiuretic hormone (PG-ADH) antagonism, operating primarily in the renal medulla. The kidney releases greatly enhanced amounts of PGE at this time, which probably act primarily in the renal medulla, then secondarily influence the systemic (arterial) levels by passing in greater amounts through the lungs. The lungs normally metabolize the major portion of PGs delivered to them. Our data suggest impairment of the lung's "up-take-metabolizing" mechanism, but also could be interpreted as involving enhanced release of PGE from the lung, so net pulmonary extraction, (V--A)/V, shifts from positive to zero or even negative values in the hypotensive shock phase. This ratio tends to improve after transfusion, but systemic PGE levels remain elevated. It is speculated that in hemorrhagic shock enhanced concentration of PGE and other vasodilator PGs, produced in increased amounts by the kidney (and possibly other organs and tissues), appear in greater amounts in the systemic plasma because of the lung's altered function. These exert a decompensatory action on the peripheral vasculature.
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PMID:Role of the kidney and lung in the handling of prostaglandin E in hemorrhagic shock. 12 27

Studies were done to investigate the transepithelial current-voltage (IT-VT) relationships of urinary bladder and colon of the toad Bufo marinus. Like several other Na transporting epithelia, the IT-VT plots characteristically showed a break at voltage E1, averaging near 124 mV for urinary bladder and 110 mV for colon. With bladders treated with antidiuretic hormone, estimates of ENa and shunt resistance, Rs, were obtained according to a method outlined by Yonath and Civan, 1971 (J Membr. Biol. 5:336-385). Our results not only confirmed their observations, but were consistent with the notion that the values of E1 (IT-VT plots) were the same as those of ENa. In addition, the values of Rs were found to be the same as those estimated from the quotient E1/I1 obtained from the voltage and current coordinates at the break of the IT-VT plot of bladders studied in both stretched and unstretched states. Amiloride at concentrations up to 10(-5) M caused a small decrease of both E1 and E1/I1 of urinary bladder. Similarly, amiloride caused small but significant changes of ENa and RNa of the colon. For both epithelia, the values of E1 and E1/I1 of the IT-VT plots were the same as those of ENa and Rs estimated by an independent method. In general, these findings are similar to those of several other epithelia where the ENa and Rs can be estimated directly from their IT-VT relationships.
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PMID:Transepithelial current-voltage relationships of toad urinary bladder and colon. Estimates of ENaA and shunt resistance. 12 55


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