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)

Arginine vasopressin, released from nerve terminals in the septal region, probably exerts endogenous antipyretic activity. A major source of vasopressin to this area is the bed nucleus of the stria terminalis (BST). In order to characterize electrophysiologically the BST-septal pathway and its potential role in the control of fever, single-unit, extracellular recordings were made from neurons in the BST of anesthetized rats. Afferent and efferent connections were identified by electrical stimulation of the medial amygdaloid nucleus and the ventral septal area (VSA). BST neurons received both inhibitory and excitatory synaptic input from the amygdala and VSA. Efferents to the VSA were identified by stimulus-evoked antidromic spike invasion. Some BST neurons were responsive to peripheral skin temperature (thermoresponsive). The activity of putative vasopressin neurons was studied during prostaglandin E1-induced fever. Although a majority of BST units was unaffected by fever, a proportion of the cells examined increased their firing rates in accordance with reported release of vasopressin in the VSA during fever.
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PMID:Single-unit activity in the bed nucleus of the stria terminalis during fever. 272 Apr 34

Male reproductive failure and infertility are quite common in alcoholics. There are very high correlations between elevated vasopressin levels and male infertility on the one hand, and probable deficiencies of prostaglandin E1 which may raise levels of PGE2 and endorphins which, in turn, release vasopressin on the other. Since head-out water immersion rapidly decreases vasopressin levels, a suggested joint protocol of head-out water immersion and a prostaglandin E-1 precursor is proposed for male reproductive failure in alcoholics.
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PMID:Vasopressin inhibition via combined head-out water immersion and a prostaglandin E-1 precursor in the treatment of male reproductive failure due to chronic alcohol abuse. 275 69

Prostaglandin E1 (PGE1) at 1 nM inhibits arginine-vasopressin (AVP)-induced water reabsorption in the rabbit cortical collecting tubule (RCCT), while 100 nM PGE1, by itself, stimulates water reabsorption (Grantham, J. J., and Orloff, J. (1968) J. Clin. Invest. 47, 1154-1161). To investigate the basis for these two responses, we measured the effects of prostaglandins on cAMP metabolism in purified RCCT cells. In freshly isolated cells, PGE2, PGE1, and 16,16-dimethyl-PGE2 acting at high concentrations (0.1-10 microM) stimulated cAMP accumulation; however, one PGE2 analog, sulprostone (16-phenoxy-17,18,19,20-tetranor-PGE2 methylsulfonilamide), failed to stimulate cAMP accumulation or to antagonize PGE2-induced cAMP formation; PGD2, PGF2 alpha, and a PGI2 analog, carbacyclin (6-carbaprostaglandin I2), also failed to stimulate cAMP synthesis. These results suggest that there is a PGE-specific stimulatory receptor in RCCT cells which mediates activation of adenylate cyclase. Occupancy of this receptor would be anticipated to cause water reabsorption by the collecting tubule. At lower concentrations (0.1-100 nM) PGE2, PGE1, 16,16-dimethyl-PGE2, and, in addition, sulprostone inhibited AVP-induced cAMP accumulation by fresh RCCT cells in the presence of cAMP phosphodiesterase inhibitors. Pertussis toxin pretreatment of RCCT cells blocked the ability of both PGE2 and sulprostone to inhibit AVP-induced cAMP accumulation. In membranes prepared from RCCT cells, sulprostone prevented stimulation of adenylate cyclase by AVP. These results suggest that E-series prostaglandins (including sulprostone) can act through an inhibitory PGE receptor(s) coupled to the inhibitory guanine nucleotide regulatory protein, Gi, to block AVP-induced cAMP synthesis by RCCT cells. Occupancy of this receptor would be expected to cause inhibition of AVP-induced water reabsorption in the intact tubule. Curiously, after RCCT cells were cultured for 5-7 days, PGE2 no longer inhibited AVP-induced cAMP accumulation, but PGE2 by itself could still stimulate cAMP accumulation. In contrast to PGE2, epinephrine acting via an alpha 2-adrenergic, Gi-linked mechanism did block AVP-induced cAMP formation by cultured RCCT cells. This implies that some component of the inhibitory PGE response other than Gi is lost when RCCT cells are cultured.
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PMID:Regulation of cyclic AMP metabolism in rabbit cortical collecting tubule cells by prostaglandins. 283 64

Prostaglandin E2 (PGE2) was found to bind specifically, reversibly, and in a protein-dependent manner to a single class of high affinity (KD approximately equal to 20 nM) binding sites in membranes prepared from canine renal outer medulla. PGE2 binding activity was solubilized from these membranes in a stable form (t1/2 greater than 14 days) in the absence of ligand in 75% yields using digitonin. The characteristics of PGE2 binding to membranes and solubilized protein were similar with respect to pH dependence, KD for PGE2, and order of potency of prostaglandins (PGE2 approximately PGE1 greater than PGF2 alpha greater than PGD2) in inhibiting the binding of [3H]PGE2. Importantly, the extents of binding of PGE2 to membranes and to a solubilized preparation partially purified by chromatography on wheat germ agglutinin-Affi-Gel 10 were both increased about 2-fold by GDP and GTP and its analogs. Treatment of the digitonin-solubilized PGE2 binding activity with 3-[(3-cholamidopropyl)dimethylammonio]-1-propanesulfonic acid (CHAPS) rendered the binding activity insensitive to stimulation by GTP and decreased the apparent molecular weight of the peak of PGE2 binding activity from about 175,000 to about 65,000. These results suggest that the PGE2 binding activity resides in a protein which is tightly associated with, but distinct from, a guanine nucleotide regulatory (N) protein. PGE2 (greater than or equal to 10 nM) was found to stimulate GTPase activity of renal outer medullary membranes, and this stimulation was eliminated by pretreatment of membranes with pertussis toxin and NAD, but not cholera toxin and NAD. Treatment of both particulate and solubilized preparations of PGE2 binding activity with pertussis toxin plus NAD also eliminated the ability of GTP to stimulate PGE2 binding. This evidence indicates that it is the inhibitory guanine nucleotide regulatory protein, Ni, with which the PGE2 binding activity is associated. Thus, this PGE2 binding activity is an inhibitory PGE2 receptor, quite possibly one that mediates inhibition of vasopressin-induced cAMP formation in the medullary thick ascending limb and/or collecting tubule of the kidney.
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PMID:Association of a solubilized prostaglandin E2 receptor from renal medulla with a pertussis toxin-reactive guanine nucleotide regulatory protein. 287 97

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

A series of analogs of vasopressin with photoreactive groups in positions 1, 2, 3, 4, 8 or 9 of the nonapeptide sequence have been studied for their effects on water and urea permeability of the isolated toad urinary bladder. Compounds with photoreactive groups in positions 3 or 8 bound covalently to receptors as judged by a persistent increase in water and urea permeability following UV irradiation, prevention of photolabeling by incubation in the presence of vasopressin, and a persistent increase in membrane-bound adenylate cyclase activity. Some analogs were inactive in the dark, but became active and bound covalently to receptors during photolysis. Other analogs were inhibitors or agonists in the dark, but did not bind to receptors following UV irradiation. Time course studies with photolabelled bladders showed a stable urea flux for 4 hr in the absence of osmotic water flow. However, in the presence of water flow urea flux was initially enhanced (solvent drag effect) and later retarded (diminished urea permeability). Binding of photoaffinity analogs to receptors was not diminished with acidification of the serosal bathing medium, lowering of the bath temperature from 21 degrees C to 4 degrees C or with addition of prostaglandin E1. However, the capacity of photoreactive analogs to effect an increase in transmural water flux, once the analog was bound covalently to receptors, was markedly diminished under these conditions.
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PMID:Action of photoreactive analogs of vasopressin in toad bladder. 293 10

Intact platelets were pretreated with hormones and thereafter membranes were prepared and Ca2+-ATPase activity determined. Thrombin decreased the Vmax of Ca2+-ATPase after pretreatment of intact platelets. Platelet activating factor, vasopressin and ADP also decreased Ca2+-ATPase activity. 12-O-tetradecanoylphorbol-13-acetate (TPA) or A23187 or ionomycin alone had no effect, whilst the simultaneous pretreatment with TPA and Ca2+-ionophore decreased Ca2+-ATPase activity. cAMP elevating agents prostaglandin E1 (PGE1) and forskolin had no influence per se on Ca2+-ATPase, but antagonized the inhibitory effect of thrombin. The data suggest a close connection between phosphoinositide metabolism and the Ca2+-ATPase system.
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PMID:The influence of activating hormones on human platelet membrane Ca2+-ATPase activity. 294 73

Paired blood samples were obtained from mothers (venous) and babies (cord venous blood) at the time of delivery by caesarean section under epidural anaesthetic. Fetal platelets failed to aggregate in response to adrenaline in vitro although adrenaline could potentiate the threshold response to adenosine diphosphate (1 microM). Fetal platelet responses to collagen and 8 Arg vasopressin did not differ significantly from maternal responses. Maternal and fetal platelets also showed similar inhibition of aggregation after activation of adenylate cyclase (PGE1 and parathormone), in contrast to the inhibition of adenylate cyclase by adrenaline. Alpha 2 adrenoceptors were investigated using [3H] yohimbine binding receptor number and were reduced modestly but significantly on fetal compared to maternal platelets. The failure of fetal platelet aggregation in response to adrenaline appears to be related to a failure of receptor coupling and may represent a delayed maturation of fetal platelet alpha receptors or a response to increased circulating catecholamines during birth.
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PMID:Maternal and fetal platelet responses and adrenoceptor binding characteristics. 298 10

Phorbol esters are tumor promoters and mitogens whose effects may be mediated by changes in ion transport across membranes. Clarification of the transport effects of these agents should be facilitated by using a well-characterized model epithelial system whose intracellular and transmural parameters are readily measurable. The current results constitute a preliminary study of the effects of 12-O-tetradecanoylphorbol-13-acetate (TPA), phorbol-12,13-dibutyrate (PDBU), and phorbol on the short-circuit current (Isc) across frog skin. TPA produced two effects: a stimulation of Isc of variable magnitude and a far more constant inhibition of the natriferic action of vasopressin. These effects appear related to the action of TPA as a tumor promoter insofar as PDBU (an active ester) also inhibited the natriferic response to vasopressin, whereas phorbol (inactive as a tumor promoter) had no significant effect. TPA is largely active from the mucosal medium, inhibits the natriferic response to adenosine 3',5'-cyclic monophosphate (cAMP) as well as that to vasopressin, and does not stimulate Isc in the presence of 10(-4) M mucosal amiloride. Inhibition of prostaglandin E1 production by indomethacin had no effect on the actions of TPA. The results indicate that frog skin is a promising model for studying the transport effects of the phorbol esters. The data further suggest that TPA acts on frog skin by activating the physiological amiloride- and cAMP-sensitive channels gating apical Na+ entry from the mucosal medium into the epithelial cells.
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PMID:Effects of tumor promoters on sodium ion transport across frog skin. 298 64

Using tritiated arginine-8-vasopressin [3H]AVP, vasopressin-specific binding sites were detected on human platelet membranes. One class of high-affinity binding sites was characterized with an equilibrium dissociation constant of 1.01 +/- 0.06 nM and a maximal binding capacity of 100 +/- 10 fmol/mg of protein (n = 12). Highly significant correlations were found between the relative agonistic (r = 0.87, P = 0.002) or antagonistic (r = 0.99, P = 0.007) vasopressor activities of a series of 13 AVP structural analogues and their relative abilities to inhibit [3H]AVP binding to platelet receptors whereas no such relationship existed when antidiuretic activities were considered (r = 0.28, P = 0.47). AVP did not stimulate cyclic AMP production of human platelets; on the contrary, high AVP concentrations (10(-6) M) inhibited cyclic AMP production measured in basal and prostaglandin E1-stimulated conditions. AVP caused intact platelet aggregation with a half-maximal aggregation (EC50) of 28 +/- 2 nM. This effect was more potently reversed by the specific vascular antagonist d(CH2)5Tyr(Me)AVP (pA2 = 8.10 +/- 0.23) than by the specific renal antagonist d(CH2)5IleuAlaAVP (pA2 = 6.67 +/- 0.12). The pA2 values of these two antagonists in platelets are in close agreement with the pKi values obtained in competition experiments (respectively 8.59 and 6.93) and with pA2 values reported in the literature for their in vivo antivasopressor activity (respectively 8.62 and 6.03). The observation that human platelets bear AVP receptors belonging to the vascular class suggests that platelet receptors can be used to further explore the role of vasopressin in cardiovascular homeostasis.
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PMID:Characterization of human platelet vasopressin receptors. 299 93


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