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)

The presence of alpha 1-receptors has been demonstrated in numerous venous fragments for various animal models. On the other hand, the presence of alpha 2-receptors in the saphenous of the dog is a matter of debate. Beta 2-receptors are activated by isoproterenol, noradrenaline and adrenaline in precontracted veins (part of the facial vein of the rabbit may be an exception). Preferential blocking by atenolol of beta 1-receptors in the jugular veins of the rat suggests that these receptors may mediate vasodilation. The saphenous veins of the dog provide the only example where specific dopaminergic receptors have been noted following partial antagonism with haloperidol. The vasoconstrictive action of acetylcholine has been seen in venous segments of numerous species and indicates the presence of muscarinic receptors. The existence of angiotensin receptors can be postulated despite the weak and inconstant in vitro and in vivo (the dorsal cerebral sinus in the dog excepted) reactions observed and the use of a non-specific antagonist. The same is true for bradykinin and vasopressin. The marked vasoconstrictive action of serotonin on all veins studied is evidence for the presence of receptors. The nature of the antagonists is subject to some divergence of opinion. Nevertheless, D tryptamine muscular receptors (or 5 HT2) can be identified due to the lack of morphine-mediated response and the efficacy of methysergide. The presence of a third type of serotoninergic receptor has only been reported once, following observations of vasodilation in the sheep. H1 receptors are involved in histamine-mediated vasoconstriction. The presence of H2 receptors which mediate vasodilation in precontracted veins remains hypothetical. Prostaglandins exhibit different efficacies in producing contraction in isolated veins; PGF2 alpha is more efficacious than PGE1 and PGE2. Prostacyclin induces contraction of human saphenous veins in a dose-dependent manner. PGE2 and particularly PGE1 can induce relaxation in precontracted veins, as is also true for prostacyclin. Receptors for these prostaglandins must exist at the post-junctional level. P2-receptors mediate transmission of the vasoconstrictive action of various purine derivatives.
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PMID:[Pharmacology of the venous system]. 288 Oct 27

The effects of lysine vasopressin (LVP) on pial arteriolar diameter and cortical periarachnoid fluid prostanoid concentrations were investigated in newborn pigs. Chloralose-anesthetized piglets were equipped with closed cranial windows over the parietal cortex for observation of pial arterioles and collection of cerebrospinal fluid (CSF) passing over the cerebral surface. Prostanoids in the CSF were determined by radioimmunoassay. LVP (10-1,000 microU/ml) elicited concentration-dependent increases in pial arteriolar diameter associated with increased levels of 6-keto-prostaglandin (PG)F1 alpha, PGE2, thromboxane B2, and PGF2 alpha. LVP-induced pial arteriolar dilation was unchanged after intravenous indomethacin (5 mg/kg). Conversely, LVP constricts pial arterioles previously dilated by physiological (hemorrhagic hypotension) and pharmacological (topically applied PGE2 or isoproterenol) intervention. This constriction is potentiated by indomethacin. Vascular and biochemical changes elicited by LVP were blocked by intravenous [1-(beta-mercapto-beta beta-cyclopentamethylene propionic acid),2,(O-methyl)-Tyr-AVP] (5 micrograms/kg), a putative V1 receptor antagonist, whereas vascular effects of norepinephrine and U46619, a thromboxane A2 mimic, were unchanged. Therefore, the degree of vascular tone appears to influence responses of the newborn pig cerebral circulation to LVP.
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PMID:Vascular responses to vasopressin are tone-dependent in the cerebral circulation of the newborn pig. 290 97

Synthesized alpha-human atrial natriuretic peptide (alpha-hANP), at 10(-6) M, failed to inhibit short-circuit current and basal and 10 mU/ml vasopressin-stimulated osmotic water flow in the bladder either pretreated with cyclooxygenase inhibitor, or preincubated with arachidonic acid, a precursor of PGE2. These results indicate alpha-hANP to have no direct effect on sodium transport and water permeability in the bladder, and no evidence was obtained indicating that alpha-hANP suppresses vasopressin-stimulated water flow by increasing PGE2 production.
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PMID:The absence of any effect of alpha-human atrial natriuretic peptide on sodium transport and osmotic water flow in the toad bladder. 293 39

PGE2 inhibited 10 m U/ml vasopressin-induced osmotic water flow of the toad bladder at 2 X 10(-8) M. PGE2 suppressed vasopressin-mediated cyclic AMP accumulation in epithelial cells and also vasopressin-mediated adenylate cyclase activity in a crude homogenate of the cells. However, PGE2 had no effect on cyclic AMP dependent and independent protein phosphorylation. These findings indicate that PGE2 inhibits vasopressin-induced water flow mainly through suppression of adenylate cyclase activity, and that the role of PGE2 at that point in the reaction leading to increased water permeability following cyclic AMP production may be slight. Under conditions in which the hormone and substrate are depleted, PGE2 and guanine nucleotides, such as GTP and Gpp(NH)p, additively bring about an increase in adenylate cyclase activity.
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PMID:The effects of PGE2 on vasopressin--and guanine nucleotide-mediated adenylate cyclase activity in toad bladder membrane. 299 18

The A23187 calcium ionophore strongly inhibits the hydrosmotic response to vasopressin. On the contrary neither exogenous cAMP nor theophylline-induced hydrosmotic response are affected by Ca++-ionophore. The effects obtained with A23187 suggest that calcium ions modulate vasopressin-induced osmotic water flow by interfering with a pre-cAMP step. The increase in intracellular calcium concentration induced by A23187, in fact, may inhibit the rate of cAMP formation by interfering with the vasopressin-stimulated adenylate cyclase system. This inhibition seems to be restricted to a locus proximal to the catalytic subunit of adenylate cyclase, whereas the hydrosmotic response to forskolin, a non-hormonal activator, is not affected by calcium ionophore addition. In order to clarify whether calcium ions act directly on the adenylate cyclase system or activate a more complex pathway, we studied the interaction between calcium and prostaglandins in modulating the hydrosmotic response to vasopressin. Direct measurements by radioimmunoassay of PGE2 release in the serosal medium show that A23187 notably increases PGE2 release. Furthermore, the inhibition of prostaglandin biosynthesis by hydrocortisone (a phospholipase inhibitor) or by indomethacin and naproxen (agents that inhibit arachidonic acid oxygenase) results in augmented vasopressin-stimulated water flow and prevents the inhibitory effect of the ionophore. Collectively these results strongly suggest that the effects obtained with A23187 on hydrosmotic response to ADH, are closely linked to calcium-stimulated PGE2 biosynthesis.
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PMID:Hydrosmotic response to vasopressin in frog skin. Control by endogenous factors. 301 Nov 58

The effect of aminoglycoside antibiotics on the response of the isolated toad urinary bladder to antidiuretic hormone (ADH) was investigated. Gentamicin and neomycin both acidify the serosal bathing solution and cause a dose-dependent inhibition of the hydroosmotic response to ADH, while streptomycin has minimal effect on media pH and causes no inhibition of the response to ADH. Detailed studies employing gentamicin indicate that acidification stimulates production of PGE2, a known inhibitor of the hydroosmotic response of the toad bladder to ADH. When media pH is rigidly controlled or PGE2 production is inhibited by indomethacin, the inhibitory effect of gentamicin on the response to ADH is ameliorated. These studies suggest that the defect in renal concentrating ability seen as part of aminoglycoside nephrotoxicity could be due, in part, to an acidification-induced, prostaglandin-mediated resistance to the action of ADH.
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PMID:Aminoglycoside toxicity: pH dependent inhibition of ADH response. 301 27

Addition of trifluoperazine (TFP) to the inside bathing solution of the isolated frog skin resulted in a biphasic increase in the short-circuit current (SCC). The Na+-flux measurements showed that the TFP-induced increase of SCC was accounted for by active sodium transport. The intracellular voltage in short circuited skins changed after addition of TFP (100 microM) from a control value of -80.9 +/- 0.8 to -66.2 +/- 1.0 mV (n = 8). This depolarization indicates that TFP acts by increasing the Na+-permeability of the apical membrane. The biphasic increase in SCC is due to different mechanisms. The primary activation could be abolished by the calcium ionophore A23187, whereas the secondary activation could be abolished by the prostaglandin synthesis inhibitor indomethacin, PGE2 or A23187. Stimulation of the SCC by TFP and theophylline or antidiuretic hormone (AVT) was additive. Furthermore, TFP did not increase the cAMP level of isolated epithelia or theophylline-stimulated epithelia. These results indicate that the TFP-induced change in the Na+-permeability was not due to an enhanced cAMP level. The TFP simulated SCC requires Ca2+ in the inside bathing solution. Addition of TFP resulted in an increase in prostaglandin E2 release to the inside bathing solution from a control value of 0.31 +/- 0.04 to 5.4 +/- 1.4 pmol PGE2 h-1 cm-2 (n = 8). It is suggested that TFP induces a Ca2+-dependent PGE2 synthesis, leading to an increase in the intracellular PGE2 concentration which might increase the Na+-permeability of the apical membrane.
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PMID:Trifluoperazine stimulated sodium transport by increased prostaglandin E2 synthesis in isolated frog skin (Rana esculenta). 301 18

Phospholipid metabolities and phospholipids containing arachidonic acid (AA) inhibited the antidiuretic hormone (ADH)-induced increase in transepithelial water flow in the toad urinary bladder, but had no effect on basal water flow when added to the serosal bathing solution. Other fatty acid-substituted phospholipid metabolites had no effect on osmotic water movement in the presence or absence of ADH. Indomethacin attenuated the inhibitory effects of the AA containing phospholipid metabolities (PMAA), suggesting that the PMAA response required AA release and prostaglandin (PG) formation. PMAA increased PGE formation as measured by radioimmunoassay. PG have been reported to inhibit ADH-stimulated water flow by inhibiting adenylcyclase. PGE2 (10(-8) M) had no effect on cyclic AMP-stimulated water flow, whereas exogenous AA and PMAA attenuated the hydroosmotic response to added cyclic AMP. Indomethacin only partially reversed the inhibition by AA of the cyclic AMP-associated water movement, suggesting that the inhibition by AA and PMAA may involve other metabolites of AA than PG. PG and the AA cascade have been implicated as cellular modulators of the ADH hydroosmotic response. The present results offer additional support to the theory that this system may regulate the intracellular events that are transduced following receptor activation by ADH.
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PMID:Inhibition of the antidiuretic hormone hydroosmotic response by phospholipids and phospholipid metabolites. 302 Mar 36

Vasopressin-prostaglandin (PG) interaction, especially the role of the inhibitory effects of PGE2 on vasopressin action, was studied using toad urinary bladders. The PGH2, at 1 X 10(-7) M, inhibited vasopressin-stimulated water flow (Marumo, 1982); PGE2 inhibited the water flow at 10(-8) M, but PGD2, PGF2 alpha, and PGI2 did not do so even at 10(-7) M. Thus, PGE2 has a physiological effect in contrast to other PGs converted from PGH2. Indomethacin enhanced both the vasopressin- and cyclic AMP-stimulated water flow across the toad bladder. However, the half maximum activation dose for vasopressin was 2 X 10(-10) M, but for cyclic AMP, as much as 3 X 10(-8) M. The PGE2 inhibited both vasopressin- and cyclic AMP-stimulated water flow. However, PGE2 inhibited vasopressin action in a dose-dependent manner which was not noted as a PGE2 effect on cyclic AMP action. The W-7, which is a specific inhibitor of calmodulin, suppressed cyclic AMP-stimulated water flow in a dose-dependent manner. Thus, PGE2 may suppress vasopressin-stimulated water flow at a site of cyclic AMP generation under physiological conditions. Thromboxane B2 (TXB2) enhanced vasopressin-stimulated water flow but not cyclic AMP-stimulated one. Thus PGE2 and TXB2 may be concluded as negative or positive modulators of vasopressin action in the toad bladder on the step(s) as the site of cyclic AMP generation under physiological conditions.
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PMID:Role of inhibitory and stimulative effects of prostaglandins on vasopressin-stimulated osmotic water flow in the toad bladder. 303 49

Arginine-vasopressin (AVP), angiotensin II (AII), and norepinephrine (NE) are known to stimulate prostaglandin (PG) synthesis in the intact rat kidney perfused with Tyrode's solution by a mechanism that requires intracellular Ca2+, while PG synthesis elicited by bradykinin (BK) is independent of Ca2+. To elucidate further the differences in the mechanism of action of BK and other vasoactive agents, in this preparation we have investigated the effect of caffeine, an agent known to interfere with the uptake and storage of Ca2+ in intracellular sites, on renal output of PGE2 and 6-keto-PGF1 alpha elicited by AVP, AII, NE, and BK; various combinations of the maximal doses of BK, AII, AVP, and NE on renal PG synthesis; and RHC 80267, an inhibitor of diglyceride and monoglyceride lipase, on the output of PGs produced by these vasoactive agents. Infusion of 1 mM caffeine inhibited PG output elicited by AVP, AII, and NE but not that caused by BK in the absence of extracellular Ca2+. Combined administration of maximal doses of BK (2.8 nmol) with that of AII (0.28 nmol), AVP (0.27 nmol), or NE (3.2 nmol) but not AVP and AII, NE and AVP, or NE and AII produced an additive effect on renal PG output in the presence or absence of Ca2+. The renal vasoconstrictor effect of AVP, AII, and NE produced in the presence of Ca2+ was not additive and remained unaltered when given together with BK.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evidence that bradykinin stimulates renal prostaglandin synthesis by a mechanism distinct from that of other vasoactive substances. 310 63


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