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 effects of various agents which have been implicated in the regulation of vasopressin release, on the supraoptic neuroendocrine cells were studied intracellularly. L-glutamate (10(-4)M) and gamma-aminobutyric acid (10(-6) M) had potent excitatory and inhibitory actions, respectively. Acetylcholine (10(-6) M) depolarized the membrane and increased the membrane input resistance. Norepinephrine (10(-5) M) produced either excitatory or inhibitory action on the spontaneous firing rate depending on the cell impaled. Morphine (10(-8)-10(-6) M) strongly depressed the spontaneous firing rate whereas it has no noticeable effect on the membrane potential and input resistance. Angiotensin II (10(-5) M) had no effect on any of the cells tested.
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PMID:Pharmacological characterization of the magnocellular neuroendocrine cells of the guinea pig supraoptic nucleus in vitro. 652 56

1. The role of intraperitoneal osmoreceptors in hypothalamo-neurohypophyseal control was studied in urethane- or nembutal-anaesthetized rats. Plasma samples were taken for radioimmunoassay of arginine vasopressin, and the electrical activity of single supraoptic endocrine neurones and of the hypothalamo-neurohypophyseal tract were monitored during superfusion of the hepatic portal vein with hypo-, iso- and hypertonic solutions. 2. Plasma arginine vasopressin increased within 1 min following superfusion with 0.3-0.9 osmolal NaCl solutions in a dose-related manner from basal levels of 30 pg/ml, to 170 pg/ml. Prior superfusion with xylocaine or intravenous infusions of 800 micrograms atropine-methyl bromate abolished this response, although vasopressin was still released to nicotine in atropine-blocked rats. 3. Portal vein superfusions had no significant effects on arterial blood pressure, plasma osmolality and plasma Na concentrations. 4. Forty supraoptic neurones were antidromically activated from the neural lobe/stalk region. Superfusions of the portal vein with NaCl solutions (0.33-1.20 osmole/kg, 37 degrees C, 5-120 sec) stimulated seven out of eight phasically firing and eight out of twenty-four continuously firing neurones. One phasically active, ten continuously firing and four silent cells were not affected, and six continuously firing neurones were inhibited by the superfusions. 5. The amplitude decreases of antidromic compound action potentials in the hypothalamo-neurohypophyseal tract, reflecting an increase of the orthodromic nerve impulse traffic, ranged from 17 to 22% for superfusions with 1.2 osmolal NaCl or LiCl solutions, from 8 to 11% for 1.2 osmolal Na isethionate or choline Cl and from 3 to 9% for 1.2 osmolal glucose; there was no effect when 1.2 osmolal urea and isotonic or hypotonic NaCl solutions were applied. 6. Responses of the amplitude of compound action potentials to superfusions with 1.2 osmolal NaCl solutions or with 0.1 mumole ACh, but not to electrical stimulation of the portal vein or its superfusion with 1.2 osmolal KCl, were abolished by prior application of 0.3 mumole atropine sulphate. Prior superfusions with xylocaine abolished the responses to all stimuli above. 7. These results suggest that within the hepatic portal vein area there are osmosensitive receptor cells and/or nerve terminals which activate the hypothalamoneurohypophyseal system through a peripheral cholinergic mechanism.
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PMID:Osmosensitivity of the hepatic portal vein area and vasopressin release in rats. 731 Jul 8

JTP-4819 ((S)-2-[[(S)-2-(hydroxyacetyl)-1-pyrrolidinyl]carbonyl]-N- phenylmethyl)-1-pyrrolidinecarboxamide) is a potent (IC50: 0.83 +/- 0.09 nM in rat brain supernatant; 5.43 +/- 0.81 nM in Flavobacterium meningosepticum) and specific inhibitor of prolyl endopeptidase (PEP). JTP-4819 (3 mg/kg p.o.) exhibited a strong and durable ex vivo inhibitory effect on PEP in various regions of the rat brain. In addition, JTP-4819 inhibited the degradation of substance P, arginine-vasopressin, thyrotropin-releasing hormone, neurotensin, oxytocin, bradykinin, and angiotensin II by purified PEP with IC50 values of 9.6, 13.9, 10.7, 14.0, 4.5, 7.6 and 10.6 nM, respectively. In the one-trial passive avoidance test in rats with scopolamine-induced amnesia, JTP-4819 significantly prolonged the retention time when administered orally at doses of 1 and 3 mg/kg 1 hr before acquisition or at 3 and 10 mg/kg 1 hr before retention. In addition, coadministration of JTP-4819 and substance P, arginine-vasopressin or thyrotropin-releasing hormone (at doses at which each drug alone did not prolong the retention time) improved the retention time of rats with scopolamine-induced amnesia. Microdialysis studies demonstrated that JTP-4819 caused a significant increase in ACh release in the frontal cortex and hippocampus of young rats at oral doses of 1 and 3 mg/kg, as well as in both brain regions of aged rats at a dose of 3 mg/kg. These results indicate that JTP-4819 potentiates neuropeptide functions inhibiting PEP, that it activates cholinergic transmission and that it enhances learning and memory.
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PMID:JTP-4819: a novel prolyl endopeptidase inhibitor with potential as a cognitive enhancer. 756 10

Calcium responses of isolated rat pineal cells to noradrenergic, cholinergic and vasopressinergic stimulations were recorded by use of the fura-2 technique and an image analysis system. Subsequently the recorded cells were identified as pinealocytes by immunocytochemical demonstration of S-antigen, a pinealocyte-specific marker. S-antigen immunoreactive pinealocytes were shown to respond to norepinephrine stimulation with an elevation of the intracellular free calcium concentration ([Ca2+]i). This response was dose-dependent and consisted of a rapid increase in [Ca2+]i (primary phase) followed by a decrease to an elevated plateau well above the basal level (secondary phase). The plateau persisted for at least 1 h when cells were constantly exposed to norepinephrine and dropped to basal level upon removal of the stimulus. Analysis of the calcium responses of cells treated with caffeine or thapsigargin suggested that the primary phase reflects mobilization of calcium from inositol 1,4,5-trisphosphate-sensitive intracellular calcium stores. Depletion of these calcium stores was a decisive and sufficient prerequisite to evoke the secondary phase which was apparently elicited by calcium influx. These data suggest that a capacitative calcium entry is involved in pineal calcium signalling. Acetylcholine induced an increase in [Ca2+]i in rat pinealocytes. Experiments with different cholinergic agonists and antagonists provided evidence that the acetylcholine-induced calcium response was mediated via nicotinic acetylcholine receptors. Stimulation of isolated rat pineal cells with arginine-vasopressin caused a rise in [Ca2+]i in approx. 5% of the cells. However, these cells remained unidentified because they contained neither immunoreactive S-antigen nor immunoreactive glial fibrillary acidic protein, a marker for interstitial (glial) cells of the rat pineal organ. Taken together, the results underline the pivotal role of norepinephrine for the regulation of pineal signal transduction, but they also support the notion that other neurotransmitters and neuropeptides are involved in the modulation of pineal calcium signalling.
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PMID:Calcium responses of isolated, immunocytochemically identified rat pinealocytes to noradrenergic, cholinergic and vasopressinergic stimulations. 758 Aug 72

The effects of vasoconstrictors on membrane potential of endothelium of intact rat aorta were investigated using the patch-clamp technique. Norepinephrine, endothelin (ET)-1, 5-hydroxytryptamine (5-HT), vasopressin, and angiotensin II evoked depolarization and oscillations in membrane potential. The alpha 1-adrenoreceptor agonist phenylephrine (PE), but not the alpha 2-agonist clonidine or the beta-agonist isoproterenol, evoked oscillations. The antagonist of 5-HT2-receptors, ketanserin, inhibited 5-HT-evoked oscillations. ET-3, unlike ET-1, did not evoke oscillations. The antagonists of voltage-operated Ca2+ channels, nifedipine and verapamil, inhibited vasoconstrictor-evoked oscillations, and the Ca2+ channel agonist BAY K 8644 enhanced oscillations. Acetylcholine and sodium nitroprusside inhibited PE-evoked oscillations. The inhibitors of NO synthase, N omega-nitro-L-arginine and NG-methyl-L-arginine, as well as methylene blue, enhanced oscillations. The intima of rat aorta with endothelium was removed from underlying smooth muscle. In this preparation, acetylcholine evoked a response similar to that in the intact vessel, but PE and ET-1 were without effect. These data suggest that vasoconstrictors acting on receptors on aortic smooth muscle evoke a response that is transferred to the endothelium and evokes depolarization and oscillations in endothelial membrane potential.
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PMID:Smooth muscle cells affect endothelial membrane potential in rat aorta. 806 36

Endothelium-dependent relaxation of mesenteric resistance arteries of spontaneously hypertensive rats (SHRs) and normotensive Wistar-Kyoto (WKY) rats was studied. Acetylcholine-induced relaxation of SHR vessels precontracted with 10 microM norepinephrine was endothelium dependent and attenuated compared with WKY vessels. The impaired response of SHR vessels was normalized by inhibition of cyclooxygenase with indomethacin. Blockade of nitric oxide synthetase with NG-nitro L-arginine methyl ester (L-NAME) or inhibition of guanylate cyclase with methylene blue attenuated acetylcholine-induced relaxation of norepinephrine-contracted SHR vessels but had no effect on WKY vessels. When vessels were precontracted with 30 nM arginine vasopressin, acetylcholine induced similar degrees of relaxation in both strains. A similar response was detected when lysine vasopressin was used to induce tone. Indomethacin had no effect on relaxation responses of SHR and WKY vessels precontracted with either form of vasopressin. L-NAME and methylene blue partially inhibited acetylcholine-induced relaxation of vasopressin-contracted vessels from both strains. Acetylcholine added at baseline did not induce contraction of vessels from either strain. It is concluded that endothelium-dependent relaxation of SHR resistance arteries is not impaired under all circumstances. Acetylcholine-induced relaxation may be suppressed in SHR resistance arteries when norepinephrine is used to induce contraction as a result of catecholamine-induced production of an endothelium-derived contracting factor. Vasopressin, on the other hand, does not elicit production of this contracting factor and may enhance the vasorelaxant action of acetylcholine in resistance arteries of both strains via actions on endothelial or vascular smooth muscle cells.
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PMID:Endothelium-dependent relaxation of hypertensive resistance arteries is not impaired under all conditions. 841 84

Stageness in the protein glands development is influenced by the nervous system mediators. Adrenergic mediation was established not to be developed by the period of provisory differentiation and appears to grow weaker by senile age. Acetylcholine stimulates growth and proliferation in the form of layers and bands. Adrenalin exerts its influence on organotypical level, which manifestates in reservation of the specific differentiation and protein type functioning of the gland. Hypothalamic neurohormones (oxytocin, vasopressin) influence the maintainance of the secretory epithelium viability.
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PMID:[The morphofunctional characteristics of the epithelium of the salivary glands and the neuroendocrine regulation of its histogenesis]. 868 39

Bile duct epithelia play an important role in the formation and conditioning of bile. However, hormonal responses in this epithelial tissue are incompletely understood. Secretin increases ductular secretion through the intracellular messenger adenosine 3',5'-cyclic monophosphate (cAMP), but whether hormones increase cytosolic Ca2+ (Ca2+(i)) in these cells and whether Ca2+(i) regulates duct secretion is unknown. To address these questions, we examined Ca2+(i) signaling in isolated rat bile duct units using ratio microspectrofluorometry and confocal microscopy. We also used videomicroscopy to examine secretion and cell volume in isolated bile duct cells and duct units. Acetylcholine (ACh) and ATP both increased Ca2+(i) in bile duct units and elicited patterns of Ca2+(i) increases and oscillations that were distinct and dose dependent. In contrast, Ca2+(i) was not increased by the hepatocyte Ca2+(i) agonists vasopressin, angiotensin, and phenylephrine or by the exocrine pancreas agonists cholecystokinin (CCK) and bombesin. In addition, secretin did not increase Ca2+(i) in the isolated bile duct units, whereas ACh did not increase Ca2+(i) in isolated hepatocytes. Mobilization of internal, thapsigargin-sensitive Ca2+ stores contributed more than influx of extracellular Ca2+ to the Ca2+(i) increases induced in the duct units, and ATP-induced increases in Ca2+(i) could be blocked by microinjection of heparin but not de-N-sulfated heparin. ACh transiently decreased bile flow in the isolated perfused rat liver, although neither ACh nor ATP altered secretion in isolated ducts or changed the volume of single isolated bile duct cells. These findings demonstrate that bile duct epithelial cells possess both muscarinic and purinergic receptors that activate Ca2+(i) signaling pathways similar to those seen in other types of epithelia, but that the two types of receptors elicit distinct patterns of Ca2+(i) signals. Increases in Ca2+(i) have minimal direct effects on bile duct secretion, although it remains to be determined whether such signals selectively modulate other aspects of bile duct epithelial cell function.
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PMID:Characterization of cytosolic Ca2+ signaling in rat bile duct epithelia. 876 Jan 11

1. Arginine-vasopressin (VP) has both vasoconstricting and vasodilating action. We report here the discovery of four novel selective hypotensive VP analogues: d(CH2)5[D-Tyr(Et)2,Arg3,Val4]AVP; d(CH2)5[D-Tyr(Et)2,Lys3,Val4]AVP and their iodinatable Tyr-NH2(9) analogues. 2. Bioassays in rats for activities characteristic of neurohypophysial peptides showed that the four VP peptides possessed little or no V1a, V2 or oxytocin (OT) receptor agonistic or antagonistic activities. 3. In anaesthetized rats, these peptides (0.05-0.10 mg kg(-1) i.v.) elicited a marked fall in arterial blood pressure. 4. Blockade of cholinoceptors, adrenoceptors and bradykinin B2 receptors, and inhibition of prostaglandin synthesis had little effect on their vasodepressor action. 5. Classical V1a, V2 and OT receptor antagonists did not block the vasodepressor response. 6. L-NAME, 0.2 mg kg(-1) min(-1), markedly suppressed the hypotensive response to ACh but not the vasodepressor response to the hypotensive VP peptides. However, the duration of the vasodepressor response was shortened. Very high doses of L-NAME attenuated both the vasodepressor response and the duration of action. 7. These findings indicate that the vasodepressor action of these VP peptides is independent of the peripheral autonomic, bradykinin and PG systems and is not mediated by the known classical OT/VP receptors. NO does not appear to have an important role in their vasodepressor action. 8. The discovery of these novel VP peptides could lead to the development of new tools for the investigation of the complex cardiovascular actions of VP and the introduction of a new class of hypotensive agents. The two iodinatable hypotensive VP peptides could be radiolabelled as potential markers for the localization of the receptor system involved.
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PMID:Discovery of novel selective hypotensive vasopressin peptides that exhibit little or no functional interactions with known oxytocin/vasopressin receptors. 983 18

Acetylcholine can stimulate the release of vasopressin. In organ-cultured hypothalamo-neurohypophyseal systems, acetylcholine enhanced vasopressin release by acting in or near the supraoptic nucleus Extracellular recordings suggested that acetylcholine can increase supraoptic neuron excitability. These effects could be mimicked, in part, by nicotine or blocked by nicotinic antagonists, suggesting that they might be mediated by nicotinic acetylcholine receptors. Autoradiography indicated that alpha-bungarotoxin binding sites are present in the supraoptic nucleus; however, neither acetylcholine nor nicotine binding sites could be detected. Thus, the existence, let alone the nature, of nicotinic receptors in the supraoptic nucleus has so far remained elusive. The present work attempts to determine: (i) whether functional nicotinic receptors are present in this nucleus; (ii) whether they are located on neurosecretory magnocellular cells or at presynaptic sites; (iii) what their pharmacological and biophysical properties are; (iv) whether they influence the activity of all or only part of supraoptic neurons. Whole-cell recordings were performed in hypothalamic slices or in acutely dissociated supraoptic neurons and the effect of nicotinic agonists was tested under voltage-clamp conditions. Autoradiography was done in coronal hypothalamic sections, using [3H]epibatidine and [125I]alpha-bungarotoxin as ligands. Our results indicate that supraoptic neurons possess functional nicotinic receptors containing the alpha7 subunit.
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PMID:Magnocellular neurons of the rat supraoptic nucleus are endowed with functional nicotinic acetylcholine receptors. 1065 10


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