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)

1. Calcium did not influence the spontaneous release of vasopressin from rat neurohypophyses in vitro when used in concentrations of 0.05, 0.5 and 2.8 mM in the bathing medium. 2. Stimulation of the basal output of vasopressin by angiotensin II (1 X 10(-9) M) required at least 0.5 mM calcium in the medium. 3. Angiotensin II stimulated the release of vasopressin within 2.5 min of incubation, maximal release was observed after 10 min. 4. Angiotensin II rapidly promoted the accumulation of tissue cyclic AMP; maximal accumulation was observed after 5 min of incubation. 5. Theophylline and dibutyryl cyclic AMP produced varying degree of stimulation of the release of vasopressin. 6. Increases in vasopressin secretion and in the accumulation of cyclic AMP were always present when neurohypophyses were exposed to optiman concentrations of angiotensin II. The results presented suggested that cyclic AMP may be an intermediate step for the release of vasopressin by endogenous angiotensin II.
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PMID:Stimulation by angiotensin II of the release of vasopressin from incubated rat neurohypophyses---possible involvement of cyclic AMP. 16 23

The effect of prostaglandin E1 (PGE1) on osmotic water flow across toad bladder and cyclic AMP content of the mucosal epithelial cells has been determined under basal conditions and in the presence of either theophylline or antidiuretic hormone (ADH); Under basal conditions and with PGE1 concentrations from 10(-8) to 10(-5) M no evidence of stimulation of water flow was observed, and with 10(-7) M PGE1 a significant inhibition was foundmcyclic AMP content under control conditions was 8 pmol/mg protein. It was 9 at 10(-8) M PGE1, 13 at 10(-7) M, 16 at 10(-6) M, and 23 at 10(-5) M. In the presence of theophylline, 10(-8) and 10(-7) M PGE1 inhibited the theophylline-induced water flow as expected. In contrast, 10(-6) and 10(-5) M PGE1 enhanced the rate of water flow. Theophylline increased cyclic AMP content from 8 to 18 pmol/mg protein. PGE1 in the presence of theophylline caused marked increases in cyclic AMP content; The content was 23 at 10(-7) M, 41 at 10(-6) M, and 130 at 10(-5) M; Thus PGE1 stimulates theophylline-induced water flow at cyclic AMP concentrations somewhere between 23 and 41 pmol/mg. Further evidence along these lines was obtained from experiments in which the effects of PGE1 on ADH-induced water flow were studied. Inhibitory effects of PGE1 were not observed at concentrations of PGE1 which raised the level of intracellular cyclic AMP to 30 pmol/mg protein or higher. These results were obtained despite the fact that all four concentrations of PGE1 tested were found capable of inhibiting ADH-induced water flow under appropriate conditions or, in other words, were inhibiting the adenylate cyclase controlling water flow, Thus the increase in cyclic AMP content in response to PGE1 is not derived from this enzyme. Thus the stimulation of water flow by PGE1 in the presence of theophylline is thought to be caused by cyclic AMP spilling over from one compartment to the water flow compartment. No evidence was obtained to directly suggest spillover into the sodium transport compartment. Furthermore evidence is discussed to suggest that most of the cyclic AMP generated in the tissue does not originate from the enzyme controlling sodium transport. As cyclic AMP-stimulated water flow and sodium transport are thought to occur in one cell type, the granular cells, distinct pools of cyclic AMP are thought to be present in one and the same cell type. Thus one pool controls water flow and one controls sodium transport. With high concentrations of PGE1 in the presence of theophylline or high concentrations of ADH, the adenylate cyclase responsible for water flow is inhibited; However, PGE1 can stimulate a tissue adenylate cyclase to sufficiently high levels that cyclic AMP spills over into the "water flow compartment" and thus stimulates water flow.
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PMID:Stimulation of osmotic water flow in toad bladder by prostaglandin E1. Evidence for different compartments of cyclic AMP. 16 31

1. Physiological concentrations of antidiuretic hormone increase diffusional water permeability but not measurable cyclic AMP content in the isolated papilla of the rat's kidney. 2. Theophylline (6 mM) increases diffusional water permeability and cyclic AMP content in the isolated papilla of the rat's kidney. 3. The increase in water permeability is detected with 5 muunits.ml-1 of ADH and is maximal with 50 muunits.ml-1. The same maximum was achieved with 6 mM theophylline. 4. Cyclic AMP and dibutyryl cyclic AMP both increase water permeability, but to a lesser extent than theophylline or ADH. 5. In the presence of theophylline, ADH causes a dose related generation of tissue cyclic AMP up to a dose of 2,000,000 muunits.ml-1. 6. Adenyl cyclase is increasingly activated by ADH up to doses of 2,000,000 muunits.ml-1. 7. These results suggest that while ADH activates the adenyl cyclase system and changes water permeability there are sufficient disparities to cast doubt on an exclusive role for cyclic AMP as the second messenger.
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PMID:The interrelationships between antidiuretic hormone, adenyl cyclase, tissue cyclic AMP and diffusional water permeability. 18 92

1. Sodium transport across isolated frog skin, as measured by the short-circuit current, was decreased by acetylsalicylic acid, mefenamic acid, paracetamol and phenylbutazone. Indomethacin (6 X 10(-6) M) had a biphasic effect on the short-circuit current: a transient increase followed by a sustained decrease. 2. The release of prostaglandin-like material from the skin was reduced by acetylsalicylic acid and indomethacin. Paracetamol caused a significant reduction in the short-circuit current response of the skin to low doses of arachidonic acid, but the response to the highest dose tested was not significantly altered. 3. Indomethacin (6 X 10(-6) M) increased the sensitivity of the skin to applied prostaglandin E1. The other prostaglandin synthetase inhibitors did not have this effect. Indomethacin (6 X 10(-6) M) also enhanced the effect of antidiuretic hormone on the short-circuit current. 4. Indomethacin (30 X 10(-6) M) increased the short-circuit current and diminished the response to applied prostaglandin E1. 5. In sulphate Ringer, theophylline increased the short-circuit current and diminished the response to prostaglandin E1. 6. Prostaglandin E1 increased the levels of cyclic AMP in frog skin and these increases preceded the increases in short-circuit current. There was a seasonal variation in the level of cyclic AMP in the skin: the levels in winter exceeded those in summer. There was also a seasonal variation in the cyclic AMP response to prostaglandin E1: the winter response was greater than that in summer. 7. Indomethacin (6 X 10(-6) M) had a biphasic effect on cyclic AMP levels in the skin, an initial increase followed by a decrease. Indomethacin also potentiated prostaglandin E1 stimulated cyclic AMP accumulation. 8. Theophylline increased cyclic AMP levels in the skin and potentiated prostaglandin E1 stimulated cyclic AMP accumulation. 9. Pre-treatment of the skin with theophylline reversed the effects of cyclic AMP on the short-circuit current and open-circuit potential. 10. It is concluded that endogenous prostaglandins help to maintain sodium transport across isolated frog skin and that the effects of E-type prostaglandins on the short-circuit current are mediated by increased cyclic AMP levels. The transient increase in short-circuit current and the increased skin sensitivity caused by indomethacin (6 X 10(-6) M) are attributed to inhibition of phosphodiesterase activity. The failure of theophylline to potentiate the short-circuit current response of the skin to prostaglandin E1 is attributed to alteration of cyclic AMP action on the skin by theophylline.
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PMID:Endogenous prostaglandins, adenosine 3':5'-monophosphate and sodium transport across isolated frog skin. 18 63

Effects of theophylline on contractions induced by relevant physiological agents in tubular segments of small human placental arteries were measured in an isometric myograph. Theophylline 10(-7) - 3 X 10(-3)M caused marked relaxation of steady contractions produced by prostaglandin F2 alpha (PGF2 alpha), prostaglandin E2 (PGE2), vasopressin or potassium. EC50 for theophylline relaxation of the PGF2 alpha - contraction was 1.6 X 10(-4) M. Emax was 91.5% relaxation. Theophylline was less potent in relaxing the potassium induced contraction. Pretreatment experiments with 10(-4) and 10(-3)M theophylline showed a pronounced decrease in contractile Emax-values for PGF2 alpha, PGE2 and vasopressin as a possible indication of non-competitive antagonism. The results motivate further studies to elucidate possible effects of theophylline and other xanthines on the vascular resistance and blood flow in placenta.
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PMID:Effects of theophylline on small human placental arteries in vitro. 385 78

The effect of prostaglandin E(1) (PGE(1)) on the water permeability response to vasopressin, theophylline, and cyclic adenosine 3',5'-monophosphate (C-AMP) of isolated, perfused collecting tubules of the rabbit was investigated in vitro. Prostaglandin is a naturally occurring substance present in a number of tissues, including kidney. It has been implicated in the action of a variety of hormones, many of which are known to exert their physiological effects through the intermediacy of the C-AMP system. In the collecting tubule, PGE(1) (10(-7) M) elicited a minimal increase in net water absorption along an osmotic gradient. However, when administered in association with a concentration of vasopressin (2.5 muU ml(-1)) selected to induce a submaximal increment in water absorption, the effect of the latter was reduced by approximately 50%. Theophylline (5 x 10(-3) M) also increased net water absorption, an effect not previously demonstrated in renal tissue. This effect was potentiated by the simulataneous addition of PGE(1). In contrast, PGE(1) did not influence the increase in net water absorption induced by C-AMP (10(-2) M). Since C-AMP is responsible for the permeability effects of vasopressin in renal tissue, the present results are consistent with the view that PGE(1) interferes with the action of the octapeptide by competing with it at a site which influences the generation of C-AMP. In addition it is proposed that prostaglandin may be an important modulator of the action of vasopressin. The tubule is exquisitely sensitive to the hormone, responding to as little as 0.25 muU ml(-1). It is conceivable that in the intact animal prostaglandin may serve to dampen the effects of small amounts of residual hormone and thereby prevent overshoots in permeability which might otherwise occur.
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PMID:Effect of prostaglandin E1 on the permeability response of the isolated collecting tubule to vasopressin, adenosine 3',5'-monophosphate, and theophylline. 429 82

1. The effects of antidiuretic hormone (ADH), theophylline and cyclic 3',5'-adenosine monophosphate (AMP) on membrane potentials in frog skin have been investigated.2. Membrane potentials across the outer and inner facing membranes were recorded in both normal and current clamped skins. In the latter condition active transport of sodium had been abolished by ouabain or metabolic inhibitors, but ionic gradients were maintained by passing current through the skin from the inside.3. ADH increases the potential across the outer facing membranes and reduces the skin resistance. The results are consistent with ADH causing an increase in permeability of the outer facing membranes to sodium ions.4. Theophylline reduces the skin potential by reducing specifically the potential across the outer facing membranes. At the same time the skin resistance is reduced. Theophylline acts by increasing the permeability of the outer facing membranes to chloride ions.5. Cyclic 3',5'-AMP causes a biphasic potential change accompanied by an increase in skin resistance.6. Metabolic inhibitors block the response of the skin to ADH but not to theophylline.7. Separate explanations for the increase in sodium transport by ADH, theophylline and cyclic 3',5'-AMP are discussed. It is not necessary to involve cyclic AMP in order to explain the effects of either ADH or theophylline.
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PMID:Independent action of antidiuretic hormone, theophylline and cyclic 3',5'-adenosine monophosphate on cell membrane permeability in frog skin. 430 35

1. Substitution of chloride by isethionate reduces the short circuit current (SCC) and increases the potential of isolated frog skin. In sodium isethionate Ringer antidiuretic hormone and choline chloride increase the SCC, whereas theophylline is ineffective.2. Frog skins treated on the outside with copper ions always show an increased potential when bathed in normal Ringer solution. The SCC may be moderately increased or decreased.3. Theophylline increases skin thickness and cell volume in non-short-circuited skins.4. The ways in which the theophylline-induced increase in chloride permeability affects sodium transport is discussed, together with the requirements for a permeant anion in both short- and open-circuited skins.
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PMID:The effects of anions on sodium transport. 576 32

1. The influence of adenosine cyclic 3',5'-monophosphate (3',5'-AMP) and of drugs believed to increase or decrease its concentration in the tissues has been determined on the response of vascular and uterine smooth muscles to catecholamines. Generally, drugs believed to increase tissue content of 3',5'-AMP potentiated the responses and those believed to decrease it depressed them.2. The cardiovascular responses of dogs (with major vessels occluded in the chest) to carotid occlusion were potentiated by infusions of theophylline and sodium fluoride. Infusion of theophylline also potentiated the response of the occluded abdominal vessels to noradrenaline.3. Intravenous infusions of theophylline and sodium fluoride potentiated pressor responses to catecholamines in the pithed rat. Infusions of iminazole depressed the responses in two animals and was without effect in two others.4. In spinal cats intravenous infusions of theophylline potentiated pressor responses to catecholamines, but sodium fluoride was without effect.5. Contractions of the isolated rat aortic strip to noradrenaline were always potentiated by sodium fluoride and by theophylline, and depressed by iminazole, when they were recorded isometrically. Theophylline always potentiated the contractions, when they were recorded isotonically but sodium fluoride was mostly, and iminazole always, ineffective.6. 3',5'-AMP in concentrations from 0.1 to 20 mug/ml. potentiated the responses of the isolated rat aortic strip to noradrenaline in thirty-eight experiments out of hundred. Concentrations from 10 to 500 mug/ml. sometimes depressed contractions recorded isometrically. In five experiments, exposure to low concentrations for 3 hr increased the resting tension of the preparation.7. Responses to noradrenaline of uteri from oestradiol-treated rabbits were potentiated by vasopressin and by sodium fluoride, but not by theophylline or iminazole. In progesterone-treated animals the responses were unaffected by vasopressin and sodium fluoride, but potentiated by theophylline and depressed by iminazole. 3',5'-AMP was without effect on the uterine responses.8. It is concluded that the results support the view that an increase in the tissue content of 3',5'-AMP potentiates the contraction of vascular and uterine smooth muscle in response to catecholamine. This view is supported by the observation that the nucleotide itself can potentiate the responses of the rat aortic strip to noradrenaline.
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PMID:The significance of adenosine cyclic 3',5'-monophosphate for the contraction of smooth muscle. 603 May 9

Theophylline (theo) induced a marked increase in the short circuit current (SCC) after maximal stimulation by the antidiuretic hormone, arginine vasotocin (AVT). The stimulation amounted to 20-70% of the AVT-stimulation. Practically no effect was seen on osmotic water flow after maximal AVT-stimulation. A concentration dependence of the SCC stimulation was found from 0.04 to 4 mM theo, 16 mM inhibited the SCC. The response to theo was independent of the time of preincubation with AVT. The theo induced increase of SCC was accounted for by active sodium transport. Theo did induce an increase in the cyclic AMP level after stimulation with a maximal concentration of AVT, but so did a supramaximal dose of AVT. This indicates that the mechanism, by which theo stimulated the SCC additional to maximal AVT stimulation, is different from that by which AVT works. This effect of theo may be unrelated to cAMP or it may be explained by differences in cellular specificity of theo and AVT.
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PMID:Theophylline-induced stimulation of sodium transport in frog skin by a mechanism different from the antidiuretic hormone activated pathway. 630 54


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