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)

Receptor-stimulated hydrolysis of inositol phospholipids was studied in atrial and ventricular myocytes isolated from guinea-pigs. Acetylcholine and carbachol stimulated inositol phosphate accumulation with a maximum of more than 12 times the unstimulated values in atrial myocytes and 7 times in ventricular myocytes. The vasoactive peptides angiotensin II and vasopressin also stimulated inositol phosphate accumulation, but the maximum effect was lower than that mediated through muscarinic receptors. However, the adenosine analogues, L-N6-phenylisopropyladenosine and 5'N-ethylcarboxamidoadenosine which, like muscarinic agonists depress cardiac contractility, did not affect inositol phosphate accumulation at concentrations up to 10(-4) mol/l. Stimulation of phosphatidylinositol turnover in heart bears no obvious relationship to either contractility or release of atrial natriuretic factor.
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PMID:Stimulation of phosphatidylinositol metabolism in the heart. 294 28

This study examined the effects of transmural nerve stimulation, acetylcholine, adrenoceptor agonists and several peptides on the contractility of strips of human gallbladder in vitro. Acetylcholine caused concentration-related contractions of the tissues and the sensitivity to acetylcholine was similar in gallbladders with mild and severe chronic cholecystitis. Noradrenaline and adrenaline relaxed gallbladder strips, probably via beta 2-adrenoceptor stimulation. Transmural nerve stimulation always caused contractions, but in the presence of atropine inhibitory responses were demonstrable and these were antagonized by propranolol. There was no evidence of non-adrenergic inhibitory neural responses. Of the peptides tested, only cholecystokinin octapeptide (CCK-OP), gastrin, pentagastrin, substance P and caerulein caused contractions. Responses to CCK-OP, gastrin and pentagastrin were antagonized by dibutyryl cyclic GMP. Hormones which had no effect upon human gallbladder strips included motilin, secretin, bombesin, neurotensin, glucagon, vasopressin, VIP and somatostatin. Considerable differences therefore exist between human tissues and those from experimental animals with respect to the direct actions of neural and hormonal stimuli on gallbladder contractility.
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PMID:Contractility of human gallbladder muscle in vitro. 297 88

1. The role of endothelium-derived relaxing factor (EDRF) in the action of vasodilator (acetylcholine, histamine, nitroprusside) and vasoconstrictor (noradrenaline, vasopressin) drugs on vascular resistance in the isolated perfused kidney and mesentery of the rat was studied. 2. Acetylcholine (EC50 = 0.18 +/- 0.05 nmol and 3.1 +/- 0.06 nmol, n = 8) and histamine (EC50 = 31.2 +/- 4.9 nmol and 46.2 +/- 3.9 nmol, n = 8) produced dose-related vasodilatation in noradrenaline-preconstricted (i.e. 'high tone') rat renal and mesenteric blood vessels. The response to both vasodilators (but not nitroprusside) was abolished by infusion of CHAPS (4.7 mg ml-1, 30 s). By use of an immunocytochemical staining procedure CHAPS was demonstrated to remove vascular endothelial cells lining intrarenal blood vessels. 3. Gossypol (3 microM), metyrapone (10 microM) and nordihydroguaiaretic acid, (NDGA, 30 microM), presumed inhibitors of EDRF biosynthesis, reduced or abolished the response to acetylcholine and histamine in perfused kidney and mesentery of the rat without affecting vasodilatation due to nitroprusside. Mepacrine (10 microM) similarly abolished the response to acetylcholine and histamine but in addition, reduced the response to nitroprusside in both preparations. 4. Methylene blue (100 microM), a presumed antagonist of the effect of EDRF, abolished vasodilatation due to acetylcholine and histamine and reduced the response to nitroprusside in perfused rat kidney and mesentery. Superoxide dismutase, SOD (15 u ml-1), was without effect. 5. While CHAPS treatment significantly augmented the vasoconstrictor response to both noradrenaline and vasopressin in perfused renal and mesenteric vessels this effect was not mimicked by metyrapone or gossypol suggesting that the enhanced effect of vasopressor agents in CHAPSperfused rat organs is due to the removal of a permeability barrier rather than impaired EDRF formation. 6. Responses to vasoconstrictor and vasodilator drugs in the perfused kidney and mesentery were obtained in the presence of indomethacin (8 microM) which produced in excess of 90% inhibition of prostacyclin (PGI2) release as measured by radioimmunoassay of 6-oxo-prostaglandin F1 alpha,. (6-oxo- PGF1 alpha) in the Krebs effluent. 7. We provide evidence that EDRF mediates the vasodilator response to acetylcholine and histamine in resistance blood vessels in perfused rat kidney and mesentery. The possibility that EDRF has a physiological role to play in regulating the calibre of resistance blood vessels is discussed.
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PMID:Endothelium-derived relaxing factor and the effects of acetylcholine and histamine on resistance blood vessels. 326 34

Effects of morphine microinjected into the hypothalamic supraoptic (SON) and paraventricular (PVN) nuclei, which contain neurons producing and releasing antidiuretic hormone (vasopressin), on the outflow and the osmotic pressure of urine and other visceral functions were investigated in a rat which was loaded with water and anesthetized with ethanol. The opioid drug, having predominantly mu-agonist activity, when microinjected into the SON or PVN induced potent antidiuretic effects in dose-dependent and time-dependent manners with no significant effects on the other visceral functions. The approx. ED50 values for morphine were 19 and 9 nmol when it was microinjected into the SON and PVN, respectively. The antidiuretic effects showed slow onset and long duration, with a minimal outflow at approx. 50 min after microinjection and a return to approx. 50% of the initial control value by 1.5 hr. The morphine-induced effects were inhibited by pretreatment with naloxone or atropine, but not inhibited by pretreatment with alpha- or beta-adrenoceptor antagonists, suggesting that the antidiuretic effects were mediated through an opioid receptor having low sensitivity to naloxone and also possibly mediated through a muscarinic receptor which was stimulated probably by the ACh released by morphine.
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PMID:Antidiuretic effects of morphine microinjected into the hypothalamic supraoptic and paraventricular nuclei in a water-loaded and ethanol-anesthetized rat. 344 15

Receptor-stimulated hydrolysis of inositol phospholipids was studied in atrial and ventricular myocytes isolated from guinea-pigs. Membrane phospholipids were labelled with [3H] inositol and their conversion to [3H] labelled inositol phosphate was measured in the presence of Li+ (10 mM). In the absence of added stimulatory hormones or neurotransmitters, little inositol phosphate accumulation was observed. Acetylcholine and carbachol stimulated inositol phosphate accumulation with a maximum of more than 12 times the unstimulated values in atrial myocytes and 7 times in ventricular myocytes. The EC50 values and 95% confidence limits for acetylcholine and carbachol were 0.9 microM (0.2 - 5.3) and 8.8 microM (6.3 - 11.8) in atria and 0.6 M (0.5 - 0.8) and 10.0 M (1.8 - 55.9) in ventricles, respectively. Oxotremorine was a partial agonist in stimulating inositol phosphate accumulation in both atrial and ventricular myocytes. The vasoactive peptides angiotensin II and vasopressin also stimulated inositol phosphate accumulation but the maximum effect was lower than that mediated through muscarinic receptors. However, the adenosine analogues, L-N6-phenylisopropyladenosine and 5'N-ethylcarboxamidoadenosine which, like muscarinic agonists depress cardiac contractility, did not affect inositol phosphate accumulation at concentrations up to 10(-4)M.
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PMID:Stimulation of phosphatidylinositol metabolism in atrial and ventricular myocytes. 378 76

Effects of methionine-enkephalin (ME) and 2-D-alanine-5-methionine-enkephalinamide (DAMEA) microinjected into the hypothalamic supraoptic (SON) and paraventricular (PVN) nuclei, which contain neurons synthesizing and releasing antidiuretic hormone, upon the outflow and the osmotic pressure of urine and the other visceral functions were studied in a rat which was loaded with water and anesthetized with ethanol. These opioid peptides when microinjected into the SON or PVN induced potent antidiuretic effects in dose-dependent and time-dependent manners with no significant effects on the other visceral functions. The approx. ED50 values for DAMEA were 1.3 (in the SON) and 0.7 (in the PVN) nmol, and the values for ME were 110 (in the SON) and 60 (in the PVN) nmol. The antidiuretic effects showed slow onset and long duration, with a minimal urine outflow at approx. 0.5 hr after microinjection and an approx. 2 hr-duration. The effects induced by the opioid peptides were inhibited by pretreatment with naloxone or atropine, without effects of pretreatment with alpha- or beta-adrenoceptor antagonists, suggesting that the antidiuretic effects were mediated through an opioid receptor having low sensitivity to naloxone and also possibly mediated through a muscarinic receptor which was stimulated probably by the ACh released by the opioid peptides.
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PMID:Antidiuretic effects of methionine-enkephalin and 2-D-alanine-5-methionine-enkephalinamide microinjected into the hypothalamic supraoptic and paraventricular nuclei in a water-loaded and ethanol-anesthetized rat. 380 52

Adrenergic and cholinergic agonists and antagonists were applied microelectrophoretically to over 700 neurons in the cat supraoptic nucleus, 20 percent of which were antidromically identified as neurosecretory cells. Norepinephrine uniformly depressed all sensitive cells. Acetylcholine caused both muscarinic depression and nicotinic excitation which were antagonized by atropine and dihydro-beta-erythroidine, respectively. These results support the hypothesis that norepinephrine and acetylcholine are directly involved in controlling the release of antidiuretic hormone.
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PMID:Supraoptic neurosecretory cells: adrenergic and cholinergic sensitivity. 439 31

1. The vessels of the isolated rabbit ear were perfused at 23 mbar with Krebs solution with (tonic) and without (atonic) noradrenaline (5.9 x 10(-7)M) at selected temperatures of 20 degrees -38 degrees C. Peripheral resistance units (PRU) were calculated from the observed peak flow rates and alterations caused by drugs expressed as Delta% PRU.2. ACh is constrictor in the atonic vessel.3. ACh is a vasodilator of the tonic vessel perfused with NA. This effect is potentiated by anticholinesterase and by denervation, unaffected by botulinum toxin and antagonized by atropine. ACh also dilates the vessel perfused with vasopressin.4. Increasing the temperature reduces the responses to ACh but increases the effect of anticholinesterase.5. Nicotine causes a dose dependent dilatation of the tonic vessels, reduced but not abolished by C(6), by atropine, by botulinum toxin and by denervation.6. Nicotine causes a dose dependent constriction of the atonic vessels, abolished by C(6) and by phentolamine, reduced by denervation, but unaffected by botulinum toxin.
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PMID:Response to acetylcholine and nicotine of the perfused vessels of the rabbit ear. 557 56

In hydrated, conscious goats nicotine was administered into the 3rd ventricle and its effects on water and electrolyte excretion were studied. Acetylcholine (ACh.) in combination with eserine (Es.) was injected by the same route in goats pretreated with atropine. Nicotine as well as large doses of Ach + Es. induced an antidiuresis of the pituitary type. The responses to ACh. were dose-dependent. Intracerebroventricular (icv.) pretreatment with hexamethonium blocked the responses to both nicotine and ACh., whereas atropine and propranolol were ineffective. It appears likely that nicotine receptors are involved inthe ACh.-induced release of antidiuretic hormone. Phentolamine (icv.) completely blocked the effects of ACh. + Es. and partly those of nicotine, indicating that catecholamines might be involved to some extent.
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PMID:Effect of intracerebroventricular injection of nicotine and acetylcholine on renal water and salt excretion in conscious goats. 611 64

Plasma vasopressin (VP) concentration is elevated in spontaneously hypertensive rats (SHRs) relative to their normotensive Wistar-Kyoto (WKY) controls. The possibility that this reflects altered responsiveness of the hypothalamo-neurohypophyseal system (HNS) in SHRs was examined by comparing VP release in response to acetylcholine from organ cultured HNS explants obtained from SHR and WKY donors. Explants were prepared from 5-, 8-, and 18-week-old animals. Blood pressure was significantly elevated in the 8- and 18-week-old SHR donors relative to their age-matched WKY donors. VP release was assessed on the 4th day of culture during a control hour and during the subsequent hour in the presence of acetylcholine. Acetylcholine caused a concentration-dependent stimulation of VP release from both types of explants, but the response was significantly greater in the explants from 5- and 8-week-old SHRs than in explants from age-matched WKYs. The explants from 18-week-old SHRs and WKYs demonstrated comparable sensitivity to acetylcholine. Basal VP release was not significantly different in explants from age-matched SHRs and WKYs, but it did increase with donor age in both strains. These studies indicate potential hyperresponsiveness of the HNS to excitatory stimuli in SHRs during the developmental phase of hypertension. The hyperresponsiveness disappears in the chronically hypertensive phase. Thus, increased sensitivity of the HNS during the development of hypertension may contribute to the elevation of plasma VP concentration in SHRs.
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PMID:Cholinergic stimulation of vasopressin release in spontaneously hypertensive rats. 651 42


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