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)

Recognition that chronologic age is not per se a cause of dementia opens the way for a more active approach to Alzheimer-type dementias as a specific disease syndrome. "Alzheimerism" in many respects is to the cholinergic brain system what Parkinsonism is to the dopamineragic. Whether cell loss or choline acetyltransferase deficiency comes first is still unclear, as is the role of vasopressin. There is a real possibility that research might produce a palliative for ACh-based defects similar to the action of L-dopa in dopaminergic defects.
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PMID:Alzheimer's disease or "Alzheimerism"? 4 21

Acetylcholine (1 and 50 mug), carbamylcholine (1 and 10 mug), and oxotremorine (10 mug) were infused into the 3rd ventricle of rats with deafferented medial basal hypothalamus (MBH); infusions failed to stimulate ACTH release as shown by the plasma corticosterone level. Implants of an atropine-fluorescein mixture (200-250 mug) inhibited the stress-induced rise of plasma corticosterone only when dye from the implant stained large portions of the median eminence and the basal hypothalamus. Atropine implants near the electrodes inhibited the rise in plasma corticosterone usually produced by electrical stimulation in the anterior hypothalamus. Atropine crystals or a 2% atropine sulphate solution placed on the median eminence blocked conduction of action potential in the hypothalamo neurohypophyseal and tubero-infundibular pathways. The evidence will be discussed for and against the participation of a cholinergic synapse (in the MBH) that activates ACTH release after stressful neural stimuli.
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PMID:The effects of cholinomimetic drugs and atropine on ACTH release. 18 78

Production, transport, storage and release of antidiuretic hormone (ADH) in the hypothalamo-neurohypophysial system were investigated. ADH produced by nerve cells in the paraventricular and supraoptic nuclei of the hypothalamus is present in a form bound to the specific protein neurophysin, in the neurosecretary granula. Electric and chemical stimulation of these nuclei results in evoked release of ADH in ionic association with neurophysin from the neural lobes. Acetylcholine, norepinephrine, histamine, angiotensin II, gamma-aminobutyric acid and L-glutamic acid have been regarded as candidates of chemical transmitters for the release of ADH in the hypothalamus. Prostaglandin (PG) E2 may be another important compound for central regulation of water metabolism. The possibility that PGE2 may be the transmitter or a modulator in the nuclei has to be considred. Serotonin, dopamine and taurine, however, may not be involded in the ADH releasing mechanisms in the hypothalamus. It appears that norepinephrine, histamine, angiotensin II, PGE2 and bradykinin stimulate directly the neural lobe to release ADH. The ADH release is regulated by intracellular Ca++. The existence of a "readily-releasable pool" of ADH can be ruled out and any limitation in the amount of ADH released under experimental conditions may be due to insufficient activation of the neural lobe. A physiological significance other than a carrier was proposed for neurophysin.
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PMID:[The hypothalamo-neurohypophysial system and antidiuretic hormone (author's transl)]. 33 45

Acetylcholine and nicotine stimulated vasopressin (VP) release from the organ-cultured rat hypothalamo-neurohypophyseal system (HNS). Nicotinic antagonists, hexamethonium, tetraethylammonium chloride, and trimethaphan blocked VP release in response to acetylcholine and nicotine. A muscarinic agonist, methacholine, was ineffective in eliciting VP release from HNS explants at a molar concentration equal to the maximally effective concentration of acetylcholine (10(-5) M). Atropine, a muscarinic antagonist, was an ineffective blocking agent for acetylcholine. These data indicate that the cholinergic receptor in the HNS explant is nicotinic rather than muscarinic in character.
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PMID:Characterization of cholinergic control of vasopressin release by the organ-cultured rat hypothalamo-neurohypophyseal system. 43 24

1. Isolated rat neurohypophyses were incubated in Locke solution at 37 degress C and the vasopressin output into the medium determined by bioassay. 2. Potassium chloride 60 mM caused a 9-fold increase in the rate of vasopressin release that was abolished when calcium chloride was omitted from the Locke solution. 3. Acetylcholine 5.5x10-4M neither alone nor in the presence of atropine 2.9x10-6M changed the "resting" release of vasopressin. 4. Neither acetylcholine 5.5x10-4M oxotremorine 10-4 and k3x10-4M altered the vasopressin release evoked by potassium chloride 60 mM. 5. In contrast to the peripheral adrenergic nerve fibres, the secretory terminal fibres of the neurohypophysis do not appear to contain muscarinic inhibitory or nicotinic excitatory receptors.
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PMID:Absence of muscarinic modulation of vasopressin release from the isolated rat neurophypophysis. 114 65

Several cholinergic processes were demonstrated and partially characterized in rabbit kidney cortical minces: choline uptake, acetylcholine synthesis and calcium-dependent release. Minces took up labelled choline, acetylated it, and stored it in a pool that was not readily accessible to physostigmine-sensitive cholinesterase activity. [3H]Acetylcholine synthesis but not [3H]choline uptake was inhibited by the removal of sodium ions or incubation at 0 degrees C. The release of newly synthesized [3H]acetylcholine was increased by 300 mOsmol urea in a calcium-dependent manner, but not by potassium depolarization (300 mOsmol), vasopressin (10 microM), or bradykinin (10 microM). These results suggest that acetylcholine may be synthesized by non-neuronal rabbit kidney cortical cells and that this transmitter may be released in response to physiological levels of urea.
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PMID:Synthesis and release of acetylcholine in the rabbit kidney cortex. 143 79

Inhibitors of nitric oxide (NO) synthesis increase blood pressure and decrease regional blood flow. We investigated whether blockade of the renin-angiotensin, sympathetic nervous, prostaglandin or vasopressin systems attenuates the effects of the NO synthesis inhibitor NG-nitro-L-arginine (L-NOARG) on mean arterial pressure and renal blood flow in anesthetized male Sprague-Dawley rats. Treatment with L-NOARG (10 mg kg-1, i.v. bolus plus infusion at 20 mg kg-1 hr-1) increased mean arterial pressure from 113 +/- 2 to 133 +/- 4 mm Hg, decreased renal blood flow from 7.7 +/- 0.6 to 4.3 +/- 0.6 ml min-1 g-1 and increased renal vascular resistance from 15.8 +/- 1.8 to 36.9 +/- 6.1 mm Hg/ml min-1 g-1. These effects were attenuated in rats pretreated with L-arginine to interfere with the inhibitory action of L-NOARG on NO synthesis, but not in rats pretreated with D-arginine. Acetylcholine did not relax aortic rings taken from rats treated with L-NOARG, consistent with inhibition of NO-mediated vasorelaxation. The pressor and renal vasoconstrictor effects of L-NOARG were not impaired in rats separately pretreated with either chlorisondamine, captopril, prazosin, indomethacin or d(CH2)5Tyr(Me)AVP, or in rats pretreated with chlorisondamine, captopril and indomethacin in combination. Collectively, these data argue against significant contribution of the sympathetic nervous system, the renin-angiotensin system, vasopressor prostanoids or vasopressin to the mechanisms of L-NOARG-induced elevation of mean arterial pressure and renal vasoconstriction in anesthetized rats.
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PMID:Pressor and renal vasoconstrictor effects of NG-nitro-L-arginine as affected by blockade of pressor mechanisms mediated by the sympathetic nervous system, angiotensin, prostanoids and vasopressin. 156 Mar 71

The relative potencies of the argininolytic agents NG-methyl-L-arginine (L-NMA), NG-nitro-L-arginine (L-NNA) and NG-amino-L-arginine (L-NAA) were assayed by their inhibitory effect on both basal and stimulated release of endothelium-derived NO in vitro and in vivo. Basal NO release was indirectly assessed by the ability of the analogs to contract phenylephrine-preconstricted rat aortic rings and their ability to produce a hypertensive response in awake, unanesthetized normotensive rats. In aortic rings, the three analogs induced vasocontraction and inhibited the vasorelaxation mediated by ACh-stimulated endothelial NO release. In this latter assay, L-NNA was 30 times more potent than either L-NMA or L-NAA. In free-moving rats, the agents caused dose-dependent increases in arterial pressure due to the blockade of endogenous NO formation. Dose-response analysis indicated that L-NNA was 87 and 230 times more potent than L-NMA and L-NAA, respectively. Pretreatment with L-NNA was also found to selectively inhibit, but not abolish, the depressor effects of acetylcholine in unanesthetized and phenylephrine- or vasopressin-infused normotensive-pithed rats. These studies indicate that L-NNA is a potent antagonist of endothelium-derived relaxing factor formation in vitro and in vivo. The contractile and hypertensive effects of the argininolytic agents clearly demonstrates that a continuous basal release of endothelium-derived relaxing factor/NO occurs in both isolated vascular rings and whole animals.
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PMID:Comparison of the inhibitory potencies of N(G)-methyl-, N(G)-nitro- and N(G)-amino-L-arginine on EDRF function in the rat: evidence for continuous basal EDRF release. 164 27

We studied whether interleukin-1 (IL-1) affects the release of arginine vasopressin (AVP) from the superfused hypothalamo-neurohypophyseal complex (HNC) of rats. Involvement of the cholinergic system in the mediation of IL-1 on AVP release from HNC was also examined. Both human recombinant IL-1 alpha and -1 beta elicited a rapid increase of AVP from HNC in a dose-dependent manner at concentrations ranging from 0.1 to 10 nM. However, neither IL-1 alpha nor -1 beta at concentrations of 100 nM increased AVP, and even suppressed the stimulatory effect of 10 nM IL-1 alpha and -1 beta added later. Acetylcholine at concentrations of 1 to 100 nM caused a dose-dependent, rapid increase in AVP, whereas AVP release induced by 10 nM acetylcholine was completely suppressed by the combined presence of 10 microM hexamethonium, a nicotinic receptor antagonist, and 50 microM atropine, a muscarinic receptor antagonist. On the other hand, AVP release induced by 10 nM IL-1 alpha and -1 beta was not affected by the combination of the two antagonists. These results suggest that both IL-1 alpha and -1 beta may stimulate AVP release by acting directly on the hypothalamo-neurohypophyseal system, and that the stimulatory effect of IL-1 on AVP release may be independent of the cholinergic system.
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PMID:Interleukin-1 (IL-1) stimulates arginine vasopressin (AVP) release from superfused rat hypothalamo-neurohypophyseal complexes independently of cholinergic mechanism. 168 90

Negative chronotropic and vasodilator responses of the isolated perfused guinea pig heart to substance P (SP) were evaluated. Bolus injections of 2.5, 25 and 125 nmol of SP caused a dose-dependent bradycardia, with the largest dose decreasing heart rate by 53% of base line. Pretreatment with 1 microM atropine blocked the negative chronotropic response to 25 nmol of SP. Pretreatment with 0.5 microM neostigmine lowered base-line heart rate and potentiated the negative chronotropic response to 25 nmol of SP. A potent vasodilator response to SP was demonstrated after elevation of base-line perfusion pressure with 1 microM [Arg8]vasopressin or 40 mM KCl. The vasodilator effect of SP was dose-dependent and occurred at much lower doses than required to affect heart rate. The ED50 for vasodilation was less than 1 pmol in both preparations. In hearts with vascular tone increased by vasopressin, atropine (1 microM) decreased the maximum vasodilator response to SP by 23%, but neither atropine nor a combination of 10 microM cimetidine and 1 microM chlorpheniramine affected the ED50 for SP. These results suggest that SP causes bradycardia by stimulating cholinergic neurons and coronary vasodilation by some mechanism not involving either acetylcholine or histamine. Acetylcholine may, however, contribute to the maximum vasodilator response to SP.
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PMID:Effects of substance P on rate and perfusion pressure in the isolated guinea pig heart. 168 42


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