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)

Four subclones of the originally cloned Harvey murine sarcoma virus-transformed Madin Darby canine kidney (MDCK) cells have been isolated. These subclones fall into two general classes. Two subclones have a fibroblastic morphology, have lost the growth requirement for prostaglandin E1 (PGE1), do not respond to glucagon or vasopressin, and, in general, appear transformed. Two other subclones have epithelioid morphologies, are growth-stimulated by PGE1, respond to vasopressin with an increase in intracellular cAMP. We propose that these cells represent revertants to a more non-transformed phenotype. Unlike normal cells, however, these revertants grow under anchorage-independent conditions, express detectable but reduced amounts of the transforming gene product, p21, and grow in nude mice. The appearance of such revertants may be one cause of the observed heterogeneity of tumor cells.
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PMID:Revertants of Ha-MuSV-transformed MDCK cells express reduced levels of p21 and possess a more normal phenotype. 300 21

Insulin stimulated the activity of a high-affinity GTPase activity in human platelet membranes some 62% over that of the basal activity. Half-maximal stimulation (Ka) was achieved with 3.1 nM insulin. The Km for GTP of the insulin-stimulated GTPase was 0.6 microM GTP. Treatment of isolated platelet membranes with cholera toxin, but not pertussis toxin, blocked insulin's ability to stimulate GTPase activity. Cholera toxin acted as a more potent inhibitor of the insulin-stimulated GTPase activity than that of the GTPase activity of the stimulatory guanine nucleotide regulatory protein, Gs, as monitored by stimulation using prostaglandin E1 (PGE1). Mixed ligand experiments showed that insulin stimulated GTPase activity in an additive fashion to GTPase activity stimulated by PGE1, due to Gs; by adrenaline (+ propranolol), due to the inhibitory guanine nucleotide regulatory protein, G1 and by vasopressin, which stimulates the putative 'Gp', a G-protein suggested to control the stimulation of inositol phospholipid metabolism. Insulin thus appears to stimulate a novel high-affinity GTPase activity in human platelet membranes. This may reflect the functioning of the putative Gins, a guanine nucleotide regulatory protein which has been suggested to mediate certain of insulin's actions on target tissues.
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PMID:Insulin stimulates a novel GTPase activity in human platelets. 303 74

The thrombin-stimulated GTPase activity of human platelets was additive with respect to the GTPase stimulation effected by prostaglandin E1, but not with that stimulated by adrenaline, vasopressin and platelet-activating factor (PAF). Treatment of platelet membranes with pertussis toxin partially inhibited the thrombin-stimulated GTPase, but had no effect on the vasopressin-stimulated GTPase activity, whereas cholera toxin treatment had no effect on either of these stimulated GTPase activities. Thrombin, adrenaline and PAF, but not vasopressin, inhibited the adenylate cyclase activity of isolated plasma membranes through the action of Ni only, this being inhibited by pertussis toxin. It is suggested that thrombin exerts effects through both the inhibitory guanine nucleotide regulatory protein Ni and through the putative guanine nucleotide regulatory protein, Np, involved in regulating receptor-stimulated inositol phospholipid metabolism. However, vasopressin appears to exert its effects solely through the putative Np.
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PMID:Thrombin, unlike vasopressin, appears to stimulate two distinct guanine nucleotide regulatory proteins in human platelets. 309 63

TPA (12-O-tetradecanoylphorbol-13-acetate) is an effective tumor promoter that affects a variety of ion transport processes. To examine the relationship between effects on transport and growth and differentiation, we have been studying the actions of TPA on frog skin, a particularly well-characterized epithelium. We have reported that high concentrations of TPA stimulate base-line short-circuit current (ISC) and inhibit the subsequent natriferic action of vasopressin. The current study of 89 preparations extends those findings. The Km of the stimulatory effect of TPA is approximately 3 nM; this high affinity indicates that the transport phenomenon does not simply reflect a nonspecific interaction of phorbol ester with the plasma membranes. TPA acts largely or entirely at the mucosal surface of both split and whole skins; thus the sidedness of the effect does not arise from adsorption onto the underlying connective tissue when TPA is applied to the serosal surface of whole skin. Amiloride, an inhibitor of apical Na+ entry, abolishes ISC across frog skins pretreated with TPA. The phorbol ester also increases ISC across split skins, preparations which do not produce net Cl-transport. Indomethacin (1 microM) blocks PGE1 release, but does not alter the response to TPA at a fivefold lower concentration than previously used. NDGA (nordihydroguaretic acid, 10 microM), an inhibitor of the lipoxygenase pathway, partially inhibited the responses of ISC to 8 nM TPA. The present results indicate that frog skin is highly responsive to TPA at concentrations known to activate protein kinase C in broken-cell preparations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of TPA on short-circuit current across frog skin. 310 64

The effect of 48 hours of water deprivation on the colonic temperature response to intrahypothalamic injection of prostaglandin E1 (PGE1) was investigated in adult male rats. Water deprivation did not alter colonic temperature of rats at a neutral ambient temperature. Administration of PGE1 at doses of 50, 200 and 400 ng gave rise to a short latency dose dependent hyperthermia in both control and water deprived rats. Water deprived rats had significantly greater increases in colonic temperature following the two higher doses of PGE1. Control rats and water deprived rats exposed to the cold (5 degrees C) had decreases in colonic temperature which were not significantly different. Water deprivation, which should increase the plasma levels of the putative endogenous antipyretic vasopressin, does not attenuate PGE1 hyperthermia but has a slight enhancing effect. Following food deprivation for 48 hours rats had a slight but significantly greater increase in colonic temperature following intrahypothalamic injection of 200 ng PGE1. Thus the water deprivation induced change in responsiveness to PGE1 may be due to the decrease in food intake which accompanies water deprivation. The mechanism by which rats exhibit an enhanced febrile response to PGE1 administration following food or water deprivation is not yet known.
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PMID:Prostaglandin E1 hyperthermia in water or food deprived rats. 337 May 2

1. Infusion of prostaglandin E1 (PGE1) into a lateral cerebral ventricle of the rat evoked a rise in core temperature which could be attenuated by electrical stimulation of the bed nucleus of the stria terminalis (BST). Electrical stimulation of the BST in the absence of PGE1 did not alter body temperature in the afebrile rat. 2. When the intracerebroventricular (I.C.V.) infusion of PGE1 was preceded by a bilateral injection of saline or vasopressin V2 antagonist d(CH2)5D-ValVAVP into the ventral septal area (VSA), electrical stimulation of the BST suppressed the PGE1 hyperthermia. However, when the vasopressin V1 antagonist d(CH2)5Tyr(Me)AVP was injected into the VSA prior to I.C.V. infusion of PGE1, electrical stimulation of the BST did not alter the hyperthermic response to PGE1. 3. These actions were site specific in that the suppression of PGE1 hyperthermia was observed only when the electrode tips were located in the area of the BST. Similarly, the V1 antagonist only blocked the effect of electrical stimulation when injected into the VSA. 4. When the vasopressin V1 antagonist was injected into the VSA, the PGE1 fever was prolonged when compared to the controls with saline. 5. Injection of saline, vasopressin V1 and V2 antagonist into the VSA, without PGE1 or BST stimulation, did not evoke any significant change in the core temperature of the rats. 6. These data are consistent with the hypothesis that vasopressin may function within the brain as an endogenous antipyretic and that vasopressin may act in a BST-VSA neuronal pathway concerned with endogenous antipyresis.
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PMID:Stimulation of vasopressin release in the ventral septum of the rat brain suppresses prostaglandin E1 fever. 340 61

The hemodynamic effects of prostaglandins PGA1, PGE1, PGE2, and PGF2 alpha on the splanchnic circulation were evaluated in five chronic dogs with portal hypertension, periportal fibrosis, and portosystemic venous shunting. The maximum effect was achieved with dosages of 2 micrograms/kg/min after bolus injection into the superior mesenteric artery. With this dosage a monophasic increase of portal blood flow and pressure was found with PGA1, PGE1, and PGE2, whereas PGF2 alpha caused a biphasic response: an initial decrease in portal blood flow and pressure was followed by an increase in these parameters. The average peak increase in portal blood flow and pressure was similar for PGE1 and PGF2 alpha, and significantly smaller for PGA1 and PGE2. Average peak iodine concentrations in the portal blood after superior mesenteric angiography were highest with PGF2 alpha, similar for PGE1 and tolazoline, and lowest in controls. The vasoconstrictor effect of PGF2 alpha is, overall, reduced and less reproducible when compared with vasopressin. This investigation suggests that both PGE1 and PGF2 alpha are effective for improved arterial portography, the latter agent appearing superior. On the other hand, PGF2 alpha cannot be recommended as a therapeutic agent for the treatment for gastrointestinal and particularly variceal bleeding.
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PMID:Prostaglandins in diagnostic and therapeutic superior mesenteric artery pharmacoangiography. 345 97

Type IIB von Willebrand's disease (vWD) is a distinct form of this disorder in which the largest multimers of the von Willebrand factor (vWF) are lacking in plasma but present in platelets. When the vasopressin analogue, 1-deamino-8-D-arginine vasopressin (DDAVP), is given to patients with type IIB vWD, an abnormal vWF is released to plasma. This vWF causes thrombocytopenia in vivo and platelet aggregation in vitro. Aggregation occurs in the plasma milieu and thus at physiological fibrinogen concentration. In this study we demonstrate that IIB post-DDAVP vWF aggregated only metabolically active platelets. The platelet aggregation was completely inhibited by EDTA and PGE1, and either inhibited or greatly weakened by ASA, demonstrating the role of divalent cations and thromboxane A2 formation. In spite of inhibiting platelet aggregation, EDTA, PGE1 and ASA did not prevent platelet binding of IIB post-DDAVP vWF. An antiserum against GP Ib made normal platelets less responsive to the IIB vWF although neither platelet aggregation nor vWF binding were completely prevented. The aggregation was fibrinogen-dependent and platelets from patients with Glanzmann's thrombasthenia were unresponsive. The studies provide evidence that IIB post-DDAVP vWF is bound to unstimulated platelets and that the interaction between vWF and platelets in type IIB vWD is different from ristocetin-induced as well as thrombin- and epinephrine-induced binding to platelets of normal vWF.
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PMID:Platelet--von Willebrand factor interactions in type IIB von Willebrand's disease. 387 38

Experiments were performed to explore the influence of (PGE1) prostagandin E1 on the local regulation of blood flow in the terminal vascular bed of the rat mesoappendix. The vasomotor activity of PGE1 on specific vascular components of the microcirculation as well as its effects on vascular responsiveness to locally applied vasoconstrictor and vasodilator agents were documented by direct in vivo microscopic observation. Locally administered PGE1 transiently dilated all muscular microvessels. Unlike the other naturally occurring vasodilator agents such as bradykinin and histamine, PGE1 antagonized the constrictor action of angiotensin, epinephrine, norepinephrine, and vasopressin long after its vasodilator activity had vanished. However, PGE1 did not interfere with the constrictor activity of serotonin, nor did it alter vascular responsiveness to the dilators, bradykinin, and histamine. Findings suggest that PGE1 may serve as a local hormonal regulator of blood flow in the microcirculation by virtue of its vasodilator properties and its ability to suppress vascular responsiveness to endogenous constrictor amines and polypeptides.
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PMID:Influence of prostaglandin E1 on the terminal vascular bed. 430 95

Synthetic [8-arginine]-vasopressin, [8-lysine]-vasopressin, [8-ornithine]-vasopressin or [2-phenylalanine, 8-lysine]-vasopressin aggregated human platelets in heparinized platelet-rich plasma. The lowest effective concentrations (1-4mU/ml) caused a primary transient aggregation, while higher concentrations also caused a secondary irreversible aggregation. Vasopressin was almost inactive in citrated platelet-rich plasma but caused aggregation in recalcified citrated or native material. Vasopressin also aggregated washed human platelets suspended in buffered saline, if fibrinogen and either Ca2+ or Mg2+ ions were present. Ethylene glycol-bis (beta-aminoethyl ether)-N,N'-tetraacetic acid inhibited aggregation completely but only after preincubation with the platelets, suggesting that platelet-bound calcium was also required. Phosphocreatine with creatine phosphokinase partially inhibited primary aggregation of platelets by vasopressin and prevented secondary aggregation, which suggests that release of platelet ADP contributed to these processes. Concentrations of vasopressin causing irreversible aggregation released small amounts of 14C from platelets containing serotonin-14C. Platelet aggregation induced by vasopressin was inhibited by adenosine, prostaglandin E1, N6,2'-0-dibutyryl cyclic 3',5'-AMP, caffeine, imipramine, or N-ethylmaleimide. Adenosine and prostaglandin E each inhibited the action of vasopressin much more powerfully than that of ADP and, therefore, cannot act solely by inhibiting the effects of the ADP released. In several respects the effect of vasopressin on blood platelets resembled its action on smooth muscle.
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PMID:Aggregation of human blood platelets by vasopressin. 434 80


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