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)

Exophthalmos has been induced in carp by injecting thyrotropin releasing hormone (TRH) (PYRO-glutamyl-histidyl-prolinamide) into the coelom. This effect was dose-dependent (dose range 5-750 mug). It was significantly potentiated by prior administration of beta-1 minus 24 coricotropin (Synacthen, Ciba) and inhibited by prednisclone. No significant increase was obtained with 2-phenylalanine-8-lysire-vasopressin (Octapressin, Sandoz). The results show that in the fish model, TRH exerts an exophthalmogenic effect by stimulating endogenous TSH, whereas in man this is not the case. They afford further evidence that the carp model does not reproduce the conditions which occur in ophthalmic Graves' disease.
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PMID:[Exophthalmogenic effect of thyrotropin releasing hormone (TRH) in the animal experiment]. 16 34

1. The effects on phosphatidylinositol metabolism of three Ca(2+)-mobilizing glycogenolytic hormones, namely angiotensin, vasopressin and adrenaline, have been investigated by using rat hepatocytes. 2. All three hormones stimulate both phosphatidylinositol breakdown and the labelling of this lipid with (32)P. 3. The response to angiotensin occurs quickly, requires a high concentration of the hormone and is prevented by [1-sarcosine, 8-isoleucine]angiotensin, a specific angiotensin antagonist that does not prevent the responses to vasopressin and to adrenaline. This response therefore seems to be mediated by angiotensin-specific receptors. 4. [1-Deaminocysteine,2-phenylalanine,7-(3,4-didehydroproline),8-arginine] vasopressin, a vasopressin analogue with enhanced antidiuretic potency, is relatively ineffective at stimulating phosphatidylinositol metabolism. This suggests that the hepatic vasopressin receptors that stimulate phosphatidylinositol breakdown are different in their ligand selectivity from the antidiuretic vasopressin receptors that activate renal adenylate cyclase. 5. Incubation of hepatocytes with ionophore A23187, a bivalent-cation ionophore, neither mimicked nor appreciably changed the effects of vasopressin on phosphatidylinositol metabolism, suggesting that phosphatidylinositol breakdown is not controlled by changes in the cytosol Ca(2+) concentration. This conclusion was supported by the observation that hormonal stimulation of phosphatidylinositol breakdown and resynthesis persists in cells incubated for a substantial period in EGTA, although this treatment somewhat decreased the phosphatidylinositol response of the hepatocyte. The phosphatidylinositol response of the hepatocyte therefore appears not to be controlled by changes in cytosol [Ca(2+)], despite the fact that this ion is thought to be the second messenger by which the same hormones control glycogenolysis. 6. These results may be an indication that phosphatidylinositol breakdown is an integral reaction in the stimulus-response coupling sequence(s) that link(s) activation of alpha-adrenergic, vasopressin and angiotensin receptors to mobilization of Ca(2+) in the rat hepatocyte.
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PMID:Phosphatidylinositol metabolism in rat hepatocytes stimulated by glycogenolytic hormones. Effects of angiotensin, vasopressin, adrenaline, ionophore A23187 and calcium-ion deprivation. 22 24

Application of information derived from a three-dimensional model of vasopressin bound to its antidiuretic receptor has resulted in the design and synthesis of a potent analog, [1-deamino, 2-phenylalanine, 7-(3,4-dehydroproline)]-arginine vasopressin; this analog has a specific antidiuretic activity of 13,000 +/- 1,250 units per milligram; noteworthy at these doses is the absence of any detectable pressor activity. Three modifications based on conformational considerations were introduced into the vasopressin molecule in preparing the analog: (i) to enhance binding, a double bond was introduced into the side chain of an amino acid residue occupying a corner position of a beta turn in the vasopressin conformation, (ii) the hydroxyl moiety was deleted from Tyr2, and (iii) to tighten the backbone structure and to enhance the enzymatic resistance of the analog, the NH2-terminal amino group was deleted.
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PMID:Vasopressin analog with extraordinarily high antidiuretic potency: a study of conformation and activity. 61 55

Pressor amine therapy in circulatory shock has been generally unfavorable, presumably because these drugs produce unselective, intense vasoconstriction and curtail rather than improve true capillary inflow, distribution and outflow in the microcirculation. The present study compares the influence of a new analog of vasopressin, [2-phenylalanine, 8-ornithine]vasopressin (POV), over wide dose ranges and Ringer's solution on: 1) survival after circulatory shock, induced by different means (e.g., hemorrhage, bowel ischemia); 2) blood pressure and hematocrit in shocked animals; and 3) various microcirculatory parameters after induction of hemorrhage and bowel ischemia shock (e.g., lumen diameters of various types of microvessels, reactivity of microvessels, microvascular flow patterns, leukocytic sticking, petechial hemorrhage formations, vasomotion, etc.). Local administration of POV, in contrast to constrictor catecholamines, induces a venular-to-arteriolar profile of constrictor activity in the normal rat mesenteric microcirculation. Systemic administration of POV to rats subjected to either lethal hemorrhage or bowel ischemia shock: 1) increases survival rates 2- to 8-fold over control rats receiving Ringer's solution; 2) produces a plateau-like effect on arterial blood pressure and returns arterial hematocrits toward normal after hemorrhage; and 3) regenerates and sustains vasomotion and venular tone, decreases microvascular hyper-reactivity characteristic of shock syndromes, restores constricted arteriolar lumen sizes toward normal, predisposes to a splanchnic microbed virtually free of stasis and petechiae, and restores capillary perfusion and outflow to near-normal. These findings indicate that it is possible to synthesize vasoactive molecules which exert selective microvascular effects and are highly beneficial in therapy of low-flow states.
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PMID:Microcirculatory approach to the treatment of circulatory shock with a new analog of vasopressin, (2-phenylalanine, 8-ornithine)vasopressin. 93 6

Reaction of tetranitromethane with the lone tyrosine residue of bovine neurophysin I and II, tyrosine-49, gave nitro derivatives of these proteins which were obtained in a highly purified form by preparative electrophoresis. Equilibrium dialysis experiments indicated clearly that oxytocin binding remained essentially unaffected by the chemical modification of tyrosine-49. However, in the case of (8-lysine)vasopressin, the nitrated protein was found to bind only 1 hormone molecule in contrast to the 2 vasopressin molecules bound by the native protein. Ultraviolet absorption difference spectroscopy measurements between 250 nm and 300 nm indicated that upon binding of (2-phenylalanine, 8-lysine)vasopressin, tyrosine-49 of native neurophysin undergoes a change of microenvironment from less to more polar surroundings. Studies of the nitrotyrosyl-49 chromophore of neurophysin by ab sorption spectroscopy in the absence and presence of oxytocin or (8-lysine)vasopressin confirmed this finding. Since dimethylsulfoxide solvent perturbation studies suggested that in the Cys(Me)-Phe-Ile-NH2-neurophysin I complex, tyrosine-49 is more exposed to solvent than in neurophysin I alone, it is concluded that this residue is unmasked by conformational changes upon complex formation.
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PMID:Interactions of bovine neurophysins with neurohypophyseal hormones. On the role of tyrosine-49. 115 Jun 56

The present study indicates that: (a) local administration of low concentrations of an analog of vasopressin, 1-deamino-[2-phenylalanine, 8-arginine]-vasopressin (DPAVP), constricts venules in the rat splanchnic terminal vascular bed of normal animals, unlike that seen for catecholamines; (b) maximal concentrations of DPAVP narrow but do not occlude both arterioles and venules: (c) microscopic muscular venules (31-39 mu i.d.) do not narrow more than 20% in response to the vasopressin analog DPAVP; and (d) terminal arterioles (17-23 mu i.d.) do not narrow more than 50% in response to DPAVP. Systemic administration of DPAVP to rats subjected to hemorrhage or bowel ischemia shock more than doubles survival rates over control rats receiving Ringer solution. Infusion of DPAVP produces a dose-dependent effect on arterial blood pressure, microscopic capacitance vessels, large arterioles and small arteries. In addition, i.v. administration of DPAVP: (a) returns arterial hematocrit towards normal after shock; and (b) regenerates and sustains vasomotion and venular tone, decreases microvascular hyperreactivity characteristic of shock syndromes, restores constricted arteriolar lumen sizes towards normal, predisposes to a splanchnic microbed virtually free of stasis, petechiae and leukocytic sticking, and restores capillary perfusion and outflow to near-normal. Further, DPAVP effectively restores the early reticuloendothelial system (RES) phagocytic depression, characteristic of shock syndromes, to normal; the latter eventuating in RES hyper-phagocytic activity. These findings indicate it is possible to synthesize vasoactive molecules which: (a) exert selective microvascular and RES phagocytic effects; and (b) are highly beneficial in the therapy of low-flow states, at least in rats.
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PMID:DPAVP: a vasopressin analog with selective microvascular and RES actions for the treatment of circulatory shock in rats. 127 38

The effect of vasopressin analogues on plasma adenosine 3',5'-cyclic monophosphate (cAMP) concentration was examined in a group of five conscious dogs instrumented for the measurement of arterial pressure and cardiac output (electromagnetic flowmeter). These dogs were infused for 20 min with a selective antidiuretic (V2) agonist, desamino-8-D-arginine vasopressin (DDAVP, 10 ng.kg-1 x min-1). This infusion was repeated on another day in the presence of the combined V1-V2 antagonist d(CH2)5-D-Tyr(Et)-4-valine,8-arginine vasopressin. The dogs also received an infusion of the selective V1 agonist 2-phenylalanine,8-ornithine oxytocin (Phe-OrnOT) at a rate of 10 ng.kg-1 x min-1. The effect of these infusions was compared with those of an isotonic saline infusion. Plasma cAMP measured in the aorta remained unchanged during all infusions but that of the selective V2 agonist DDAVP alone, during which it increased significantly from 22.4 +/- 0.8 to 32.6 +/- 4.6 and 37.0 +/- 4.1 pmol/ml after 10 and 20 min, respectively. In the plasma sampled from the inferior vena cava caudal to the renal veins, cAMP increased during DDAVP infusion from 22.2 +/- 2.5 to 39.2 +/- 3.8 and 36.0 +/- 4.0 pmol/ml after 10 and 20 min, respectively. The infusion of DDAVP was later given to the same dogs under anesthesia after bilateral nephrectomy, which did not modify the effect of DDAVP on arterial plasma cAMP. In another group of four conscious dogs, infusion of DDAVP at the same rate did not induce significant changes in plasma catecholamines.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:cAMP and extrarenal vasopressin V2 receptors in dogs. 133 16

The isolated rat hindquarter preparation perfused at constant flow was used to determine resistance and capacitance responses from pressure and weight recordings. In response to noradrenaline at low concentrations, the capacitance effect was greater than the relative increase in total vascular resistance. 8-L-Arginine vasopressin showed capacitance responses only when the resistance vessel constriction was pronounced. Oxytocin and two synthetic analogues, 2-phenylalanine-8-ornithine vasopressin (Phe-Orn-VP) and 2-phenylalanine-8-ornithine oxytocin, showed varying potency for resistance vessel constriction but hardly any capacitance responses. However, when Phe-Orn-VP induced a small increase in total vascular resistance, a marked increase in post-capillary resistance was observed. The results are discussed in relation to a study in which the effects of vasopressin analogues were studied with intravital microscopy (Altura 1973).
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PMID:Effects of noradrenaline and vasopressin analogues on resistance and capacitance vessels in the rat hindquarter preparation. 235 60

Vasotocin (AVT) analogues with tyrosine or phenylalanine in position 9, i.e., [9-tyrosine]AVT, [2-phenylalanine,-9-tyrosine]AVT, and 1-desamino[9-(p-aminophenylalanine)]AVT, were synthesized by the solid-phase method. These compounds showed a high biological activity in the hydroosmotic toad bladder assay. Using the chemically reactive functional groups on tyrosine and p-aminophenylalanine in position 9, we prepared iodinated, photoreactive, and affinity ligands, i.e., [2-phenylalanine,9-(iodotyrosine)]AVT, 1-desamino[9-(p-azidophenylalanine)]AVT, and 1-desamino[9-(biotinylphenylalanine)]AVT, respectively. Half-maximal hydroosmotic responses (ED-50 values) were obtained with 2.5 X 10(-9) M for the iodinated analogue, with 0.9 X 10(-10) M for the photoaffinity analogue, and with 1.2 X 10(-8) M for the biotinyl analogue. The hydroosmotic activity of the biotinyl analogue was reversed following addition of avidin, whereas the photoaffinity analogue induced a persistent response following UV irradiation that was not reversed upon repeated and prolonged periods of washout. These analogues of vasotocin are the most potent that have been synthesized to date, and they should serve as useful probes in the isolation and characterization of vasotocin receptors in toad bladders and tissues from other species that use vasotocin as an antidiuretic/pressor principle. The photoaffinity and biotinyl analogues had a rat antidiuretic activity of 66 and 40 units/mg, respectively. These compounds are, therefore, also suitable for the isolation of V-2 vasopressin receptors from mammalian tissues.
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PMID:Photoaffinity, biotinyl, and iodo analogues as probes for vasotocin receptors. 281 Mar 31

Extracellular recordings were obtained from single neurons located in the lateral septum, an area known to receive a vasopressinergic innervation in the rat brain. Approximately half of the neurons tested responded to 8-L-arginine vasopressin (AVP) by a marked increase in firing rate at concentrations greater than 1 nM. The effect of vasopressin was blocked by synthetic structural analogues possessing antagonistic properties on peripheral vasopressin and oxytocin receptors. Oxytocin was much less potent than vasopressin in firing septal neurons, and a selective oxytocic agonist was totally ineffective. The action of vasopressin on neuronal firing was mimicked by the vasopressor agonist [2-phenylalanine,8-ornithine]vasotocin but not by the selective antidiuretic agonist 1-deamino[8-D-arginine]vasopressin. In a parallel study, sites that bind [3H]AVP at low concentration (1.5 nM) were found by in vitro autoradiography in the lateral septum. Adjacent sections were also incubated with 1.5 mM [3H]AVP and, in addition, with 100 nM [2-phenylalanine,8-ornithine]vasotocin or 1-deamino[8-D-arginine]vasopressin--i.e., the same compounds as those used for the electrophysiological study. Results showed that the vasopressor agonist, but not the antidiuretic agonist, displaced [3H]AVP, thus indicating that the vasopressin binding sites detected by autoradiography in the septum were V1 (vasopressor type) rather than V2 (antidiuretic type) receptors. Based on the electrophysiological evidence, we conclude that these receptors, when occupied, lead to increased firing of lateral septal neurons.
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PMID:Electrophysiological and autoradiographical evidence of V1 vasopressin receptors in the lateral septum of the rat brain. 295 62


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