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)

Vasopressin increases the net transport of sodium across the isolated urinary bladder of the toad by increasing the mobility of sodium ion within the tissue. This change is reflected in a decreased DC resistance of the bladder; identification of the permeability barrier which is affected localizes the site of action of vasopressin on sodium transport. Cells of the epithelial layer were impaled from the mucosal side with glass micropipettes while current pulses were passed through the bladder. The resulting voltage deflections across the bladder and between the micropipette and mucosal reference solution were proportional to the resistance across the entire bladder and across the mucosal or apical permeability barrier, respectively. The position of the exploring micropipette was not changed and vasopressin was added to the serosal medium. In 10 successful impalements, the apical permeability barrier contributed 54% of the initial total transbladder resistance, but 98% of the total resistance change following vasopressin occurred at this site. This finding provides direct evidence that vasopressin acts to increase ionic mobility selectively across the apical permeability barrier of the transporting cells of the toad bladder.
J Gen Physiol 1968 May
PMID:The site of the stimulatory action of vasopressin on sodium transport in toad bladder. 565 1

A sensitive and precise method for assaying the water permeability response evoked by neurohypophyseal hormones and their synthetic analogues on the isolated urinary bladder of the toad (Bufo marinus L.) is described. The method permits detection of 8-arginine-vasotocin at concentrations as low as 10(-12)M. This sensitivity, not achieved heretofore with this tissue, results largely from minimizing interference of inhibitory substances by means of an "in vitro circulation assembly." The precision of the method derives from a direct comparison between the cumulative dose-response curve of an agonist of unknown potency acting on one hemibladder and that of a reference compound acting on the contralateral hemibladder. Crystalline deamino-oxytocin is used as the reference standard in this assay. The intrinsic activity of 2-(O-methyltyrosine)-oxytocin, as defined by the maximal response, is 12% lower than that of deamino-oxytocin. All other hormonal peptides investigated have the same intrinsic activity as deamino-oxytocin, even 5-valine-oxytocin, in spite of its extremely low affinity. A comparison of the potencies of 8-arginine-vasotocin vs. 8-arginine-vasopressin, 8-ornithine-vasotocin vs. 8-ornithine-vasopressin, 8-alanine-oxytocin vs. 8-alanine-oxypressin, and deamino-8-alanine-oxytocin vs. deamino-8-alanine-oxypressin suggests that an isoleucine residue in position 3 imparts a higher specificity for binding of the hormonal peptide molecule to the bladder receptor than a phenylalanine residue in this locus.
J Gen Physiol 1968 Sep
PMID:A sensitive hydroosmotic toad bladder assay. Affinity and intrinsic activity of neurohypophyseal peptides. 569 11

The isotopic equilibration of urea, thiourea, and inulin between urine and plasma was determined in rabbits in the presence or absence of antidiuretic hormone (ADH). Animals were anesthetized with ethanol and permitted to reach steady state after completion of surgery. Tracer was then administered by intraarterial infusion in such a manner that a high constant specific activity in plasma was rapidly attained. Urine flow was kept independent of ADH by addition of mannitol. Urea/creatinine clearance ratios and the accumulation of urea in renal medulla and papilla also remained unaffected by ADH. Under these conditions, thiourea and inulin at all times approached equilibrium, at similar rates. In the absence of ADH, urea also equilibrated at a rate similar to that of inulin. The addition of ADH, however, significantly prolonged the delay before urinary urea reached the high constant specific activity of plasma urea. These observations are interpreted in terms of a specific effect of the hormone on the solute permeability of the nephron.
J Gen Physiol 1966 Sep
PMID:The action of pitressin on solute permeability of the rabbit nephron in vivo. 597 Oct 28

The synthetic analogue of vasopressin, 1-deamino-8-D-arginine-vasopressin (dDAVP), possesses a protracted antidiuretic activity while having practically no pressoric activity as compared to arginine-vasopressin (AVP) or lysine-vasopressin (LVP). The effects of LVP and dDAVP were studied on the frog skin (Rana temporaria) sodium transport as reflected by the short-circuit current (SCC) level, on an Ussing apparatus. The application two different equimolar doses of LVP or dDAVP (approx. 9.4 X 10(-8) mol X l-1 and 18.8 X 10(-8) mol X l-1 to the inner surface of the skin resulted in identical maximal increases of sodium transport. However, the maximum transport stimulation after the application of dDAVP was delayed by about 30 min as compared to the stimulation by LVP (P less than 0.01). In addition, a protracted recovery of SCC towards its original levels was observed in experiments with dDAVP application after the hormone removal (P less than 0.01). It is concluded that dDAVP stimulates Na+ transport through the frog skin despite its lacking pressoric activity. Thus, the natriferic activity of vasopressin is related to its antidiuretic rather than pressoric activity. Maximum increase in the sodium transport following dDAVP application was delayed and more protracted as compared to the effect of LVP.
Gen Physiol Biophys 1984 Aug
PMID:Effects of lysine-vasopressin (LVP) and 1-deamino-8-D-arginine-vasopressin (dDAVP) upon electrical potential, short-circuit current and transepithelial D.C. resistance of the frog skin. 609 99

In in vitro cultures of liver from Ambystoma mexicanum glycogenolysis was stimulated by adrenaline, glucagon, and vasopressin in a dose-dependent manner. Maximum activity was seen at 10(-6) M hormone while 10(-9) M was without effect. Dibutyryl cyclic AMP (10(-3) M) stimulated glycogenolysis maximally although 10(-5) M had no effect. The glucose release brought about by adrenaline was blocked by the beta-adrenergic antagonist propranolol but not by prazosin or yohimbine which are alpha 1- and alpha 2-adrenergic antagonists. Cyclic AMP concentrations in liver were elevated within 1 min of administration of adrenaline and remained elevated for at least 60 min. Phosphorylase a activity was elevated 10 min after addition of adrenaline and remained elevated for at least 6 hr. The rise in hepatic cyclic AMP concentration and phosphorylase a activity was largely blocked by propranolol. These findings are consistent with adrenaline acting via a beta-adrenergic receptor in A. mexicanum. Glycogenolysis in A. mexicanum liver was stimulated by isoprenaline and phenylephrine and in each case the stimulation was reduced in the presence of propranolol but unaffected by phentolamine. High concentrations of methoxamine, a specific alpha 1-agonist, had no effect upon glycogenolysis. These findings suggest that alpha-adrenergic receptors play no role in regulation of glycogenolysis in A. mexicanum.
Gen Comp Endocrinol 1983 Mar
PMID:Hormonal control of glycogenolysis and the mechanism of action of adrenaline in amphibian liver in vitro. 630 36

To study the mechanisms by which antidiuretic hormone and prostaglandins regulate Na transport at the apical membranes of the cells of anuran tissues, studies were done with fluctuation analysis. Epithelia of frog skin (Rana pipiens) were treated with vasopressin alone, or treated with vasopressin after inhibition of Na transport by indomethacin. The tissues were bathed symmetrically with a Cl-HCO3 Ringer solution and short-circuited continuously. In this experimental circumstance, the amiloride-induced current noise power density spectra were of the Lorentzian type with little or no l/f noise, provided that "scraped" skins were used for study. Despite large changes of Na transport, especially in epithelia treated with indomethacin and vasopressin, the single-channel Na current remained essentially unchanged, whereas the density of amiloride-inhibitable, electrically conductive Na channels was increased by vasopressin and decreased by indomethacin.
J Gen Physiol 1983 Aug
PMID:Hormonal control of apical membrane Na transport in epithelia. Studies with fluctuation analysis. 631 38

Adrenergic effectors were shown to play a major role in increasing cutaneous water uptake (the hydroosmotic response) in dehydrated anurans. A beta-adrenergic antagonist, propranolol, blocked 61% of the cutaneous response to dehydration and 67% of the response elicited by salt loading in the toad Bufo cognatus. A beta-adrenergic agonist, isoproterenol, elicited a response in normally hydrated animals equal to the propranolol-sensitive portion of the cutaneous hydroosmotic response of dehydrated animals. The isoproterenol-induced cutaneous water balance response in hydrated animals greatly exceeded the response induced by arginine vasotocin, the endogenous antidiuretic hormone.
Gen Comp Endocrinol 1984 Feb
PMID:Adrenergic control of the anuran cutaneous hydroosmotic response. 632 Dec 96

The influence of different neuropituitary hormones on the contraction of the Brazilian opossum uterus in vitro was studied in spayed adults injected with (i) peanut oil (ii) estrogen or (iii) estrogen plus progesterone, and in a fourth group of lactating animals. Two parameters were analyzed from the dose-response curve: pD2 and the relative contractile response compared to the maximal one induced by oxytocin. When oxytocin was administered to the bath, neither pD2 nor the contractile force was affected by any hormonal treatment or lactation. Oxytocin, however, remained in any hormonal status, the most powerful agonist to induce uterine contraction. Lysine vasopressin was the weaker agonist in any hormonal status. It binds slightly less to the isolated uterus than to the hormone-treated one. The maximal contractile force remains unchanged when the uterus is from ovariectomized or steroid-treated animals. However, after lysine vasopressin, uterus from lactating opossum develops a less intense contractility than that observed in other groups. Arginine vasopressin induces a contractile force comparable to that induced by oxytocin in any hormonal status. The affinity of this peptide for the uterine receptor is significantly lower in ovariectomized and estrogen-treated animals; after progesterone injection or in lactating animals the receptor affinity for this hormone is increased to the level of the affinity for oxytocin. Receptor affinity for arginine vasotocin is reduced in any hormonal state and brought to a level comparable to that for oxytocin only in lactating animals. On the other hand, progesterone reduced the maximal contractile force induced by this neuropeptide.(ABSTRACT TRUNCATED AT 250 WORDS)
Gen Comp Endocrinol 1984 Jan
PMID:Influence of estrogen and progesterone on the uterine sensitivity in vitro to neuropituitary hormones in the Brazilian marsupial Didelphis albiventris: comparison with lactating animals. 632 93

The cAMP level in isolated frog skin epithelia was stimulated by a range of concentrations of the antidiuretic hormone arginine vasotocin (AVT) and compared to active sodium transport measured as short-circuit current (SCC). The response of SCC and osmotic water flow (OWF) to AVT was investigated in a separate series. SCC was approximately three times more sensitive to AVT than OWF. Measurable increments of cAMP above the basal level were found only with AVT concentrations eliciting half-maximal response or more of SCC. Two models are offered to explain the findings: (A) Total SCC depends on epithelial cAMP with a sigmoidal relationship. (B) Epithelial cAMP exists in two separate pools of which only one is accessible to AVT, and SCC stimulation depends on cAMP in the AVT-controlled pool in a simple saturable fashion. Correlation between cAMP and SCC after stimulation with theophylline resembled that after AVT. Papaverine (10 microM) induced only small changes in SCC inspite of a substantial increase in cAMP level. Higher concentrations of papaverine inhibited both basal and AVT-stimulated SCC, while the cAMP level was further increased. This effect of papaverine may be due to a simultaneous block of another rate-determining process. Papaverine had no effect on basal or AVT-stimulated OWF despite a marked stimulation of the cAMP level. Thus, the role of cAMP as mediator of the hydroosmotic action of AVT must be questioned.
Gen Comp Endocrinol 1984 Apr
PMID:Correlation between cAMP in isolated frog skin epithelium and stimulation of sodium transport and osmotic water flow by antidiuretic hormone and phosphodiesterase inhibitors. 632 59

V1 vasopressin, angiotensin, alpha-adrenergic, and glucagon receptors in liver were studied on membrane fractions prepared from two groups of jerboas ( Jaculus orientalis) given dry or water-enriched diets for periods of 4 to 7 weeks, and from rats acutely treated with pharmacological amounts of arginine-vasopressin (AVP) or (1-deamino-8-D-arginine)-vasopressin (dDAVP). Tritiated (8-lysine)-vasopressin ([3H]vasopressin), tritiated (1-asparagine-5-valine)-angiotensin II ([3H]angiotensin II), tritiated dihydroergocryptine ([3H] DHEC ), and iodinated glucagon ([125I]-glucagon) were used as specific labeled ligands of these receptors. The V1 vasopressin, angiotensin, alpha-adrenergic, and glucagon receptors detected in both groups of jerboas were identical to receptors found in rat liver plasma membranes in regard to the apparent dissociation constants for their respective labeled ligands. Furthermore, vasopressin receptors in jerboa liver membranes discriminated as efficiently as rat liver receptors between the natural neurohypophyseal peptides arginine-vasopressin and lysine-vasopressin on the one hand and the structural analogs (1-deamino-8-D-arginine)-vasopressin and (4-valine-8-D-arginine)-vasopressin on the other. The reduction of antidiuretic hormone (ADH) secretion in jerboas fed a water-enriched diet compared to those on a dry diet (75 +/- 25 pM versus 372 +/- 86 pM) was accompanied by an increase in the number of liver vasopressin receptors (2.79 +/- 0.53 versus 1.25 +/- 0.14 pmol [3H]vasopressin bound/mg protein). The modifications observed were specific for vasopressin receptors, as judged by the maximal binding capacities of [3H]angiotensin II, [3H] DHEC , and [125I]-glucagon, which remained unchanged in jerboas whatever the levels of endogenous circulating ADH. Similarly, administration of pharmacological doses of AVP by iv infusion to rats induced, 2 hr later, a loss of about 50% of V1 liver vasopressin receptors, while the numbers and apparent dissociation constants of angiotensin, alpha-adrenergic, and glucagon liver receptors remained unchanged, and V2 kidney vasopressin receptors were almost desensitized. For V1 liver and V2 kidney vasopressin receptors, the desensitization process was strikingly dependent on the antidiuretic/glycogenolytic activity ratio of the peptide used. Thus, im injection to rats of dDAVP (an analog possessing a very high antidiuretic/glycogenolytic activity ratio) induced, 1 hr later, a total loss of V2 kidney receptors without modification of the number and apparent dissociation constant of V1 liver receptors.
Gen Comp Endocrinol 1984 May
PMID:Plasma antidiuretic hormone levels and liver vasopressin receptors in the jerboa, Jaculus orientalis, and rat. 632 98


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