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)

Dopamine (DA) and noradrenaline (NA) levels and activities of the enzymes metabolizing catecholamines were determined in the rat brain and kidneys during prolonged (4 weeks) administration of lysine vasopressin (LVP) and 2 weeks after its withdrawal. DA level was elevated during the whole period of experiment. NA level increased mainly after LVP withdrawal. Dopa-decarboxylase activity was elevated in all the experimental animals. Tyrosine and dopamine-beta-hydroxylase activities increased at the final period of LVP administration and after its withdrawal. Activities of MAO and COMT were markedly increased only after 3 weeks of LVP administration.
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PMID:The effect of prolonged vasopressin administration on the level and metabolism of catecholamines in the rat brain and kidneys. 0 18

The "DOPA potentiation" test in mice was investigated for its usefulness in the detection of compounds with antidepressant properties. It was found that the anti-depressant drugs imipramine, amitriptyline, 5-methylamino-acetyl-6-methyl-5,6-dihydro-phenanthridine-HCl (Org OI77) and 1,2,3,4,10,14b-hexahydro-2-methyl-dibenzo[c,f]pyrazino[1,2-a]azepine-HCl (mianserin, Org GB 94) potentiated the behavioural effect of DOPA in groups of mice which had been treated 17 h previously with the monoamine oxidase inhibitor (MAOI) iproniazid. However, the DOPA response was also potentiated by a variety of centrally acting drugs which do not have antidepressant properties (atropine, methysergide, chlordiazepoxide, apomorphine). The peptide hormones ACTH4-10 and desglycinamide lysine vasopressin had equivocal effects while melanocyte stimulating hormone release-inhibiting factor (MIF) had no effect on the DOPA response. The DOPA response was inhibited by the neuroleptics chlorpromazine and haloperidol. There appeared to be no correlation between the effects of the drugs on the behavioural responses elicited by DOPA and the changes found in the brain concentration of noradrenaline, dopamine, serotonin, gamma-aminobutyric acid, tryptophan and tyrosine. It is concluded that the "DOPA potentiation" test cannot be considered as a reliable test in the detection of anti-depressant compounds.
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PMID:The action of psychotropic drugs on DOPA induced behavioural responses in mice. 1 9

In order to study the control of vasopressin-release, the effect of a series of potential agents was studied in an in vitro perifusion system of rat neurohypophysis after in vivo treatment with nialamide, a monoamine oxidase inhibitor. In this system, metlatonin stimulated vasopressin-release in a dose-dependent manner (1 x 10-8 to 1 x 10-3 M). Serotonin (1 x 10-3 M) also led to a significant increase of vasopressin-release whereas quipazine (1 x 10-3 M), a putative serotonin agonist and monoamine oxidase inhibitor, caused a 3-fold stimulation of the release of the neurohormone. The stimulatory effects of melatonin and serotonin were prevented by omission of Ca2+ combined to an excess of Mg2+ (12mM) in the perifusion medium. 1 x 10-6 M somatostatin did not affect basal or melatonin-stimulated vasopressin-release. These results show that melatonin and serotonin can have a direct stimulatory effect on vasopressin release at the neurohypophyseal level.
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PMID:Melatonin-and serotonin-stimulated release of vasopressin from rat neurohypophysis in vitro. 46 80

Varying degrees of monoamine oxidase (MAO) activity were noticed all along the hypothalamo-hypophyseal neurosecretory tract in C. batrachus. Intense activity was evident on the wall of the secretory cells of the adenohypophysis, neurons of the nucleus preopticus (NPO) and nucleus lateralis tuberis (NLT). However, MAO activity was also observed in the cytoplasm of some neurons in the ventromedian region of the NLT and groups of cells present in the neurohypophyseal ramifications of the pars intermedia. A strong accumulation of formazan granules in the median eminence (ME) and the neuroadeno interface lends further support to the view that C. batrachus has a ME of both the tetrapodan and the teleostean type. The distributional pattern of MAO in the hypothalamus and hypophysis suggests that monoaminergic fibres are probably involved in the secretory mechanism of the releasing factors and pituitary hormones.
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PMID:Distribution of monoamine oxidase (MAO) in relation to the hypothalamo-hypophyseal system of the teleost Clarias batrachus (L.). 97 96

Experiments on rat mesenteric arterioles, metarterioles, and aortae demonstrate that although alpha-methylnorepinephrine is much less potent in inducing contraction than epinephrine on all three blood vessel types, it is either equivalent or only one and a half to two times less potent than the natural postganglionic neurotransmitter, norepinephrine, on these blood vessels. Furthermore, alpha-methylnorepinephrine is equivalent to norepinephrine in its ability to induce maximal contractile responses on rat arterioles, metarterioles, and aortae. Systemic administration of alpha-methyldopa to rats for 15 days shifted the log dose-response curves for all three catecholamines, but not vasopressin or potassium chloride, to the right of all three blood vessel types; the maximal contractile responses to these amines were, however, not affected by chronic treatment with alpha-methyldopa. In addition, acute, intra-arterial administration of 500 mg/kg of alpha-methyldopa was found not only to induce mesenteric arteriolar vasodilatation gradually but also to depress arteriolar reponsiveness to catecholamines. In view of these direct findings, it is difficult to accept the hypothesis that alpha-methyldopa induces hypotension via formation of a "false" postganglionic neurotransmitter substance, namely, alpha-methylnorepinephrine. The present findings suggest that alpha-methyldopa may exert some of its anti-hypertensive action, at least in the rat, by (1) depressing arteriolar responsiveness to circulating and released catecholamines and (2) some unknown direct action on peripheral vascular muscle. In addition, the present study indicates that octopamine is (1) between 60 and 15,000 times less potent than norepinephrine on rat arterioles and metarterioles and (2) incapable of eliciting more than a 40% occlusion of these terminal vessels. It is suggested that such data support the concept that octopamine, in contrast to alpha-methylnorepinephrine, could serve as a false adrenergic neurotransmitter agent and thus account for part or all of the hypotensive action of monoamine oxidase inhibitors like pargyline. The use of complete dose-response curves, several different adrenergic compounds (i.e., epinephrine, norepinephrine, alpha-methylnorepinephrine, octopamine, phenylephrine, and dopamine), and different rat blood vessels supports the concept that adrenergic molecules containing a catecholamine nucleus and a beta-hydroxyl group elicit the most potent constrictor responses from peripheral blood vessels. In addition, the data suggest that the structure-activity relationships for catecholamines and their analogs on terminal vascular smooth muscle are probably different from those for arterial smooth muscle.
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PMID:Pharmacological effects of alpha-methyldopa, alpha-methylnorepinephrine, and octopamine on rat arteriolar, arterial, and terminal vascular smooth. 109 55

Trapymin (TM) relaxed excised renal, coronary, pulmonary, femoral and mesenteric arteries and this relaxation was not antagonized by propranolol. The dose-response curve of TM was parallel to that of nitroglycerin and papaverine and steeper than that of dipyridamol or adenosine. TM exerted inotropic and chronotropic actions on excised rat atrium. TM was also effective through the oral route and the effectiveness tended to decrease slightly after repeated use for ten days. TM was effective on vasopressin induced angina in rats and electrocoagulation-induced myocardial infarction. TM suppressed adrenaline-induced arrhythmia but not CaCl2-induced arrhythmia. TM reduced catecholamine content in brain, adrenals and heart but had no influence on monoamine oxidase or dopamine-beta-hydroxylase. TM revealed ganglion-blocking and neuron-blocking actions in cervical ganglion in cats. With propranolol, TM-induced hyperglycemia and reduction in glycogen content in liver and heart was antagonized but TM-induced rise in free fatty acid in serum was not antagonized. Na+-K+ dependent ATPase of bovine heart and P/O ratio of mitochondria of rat heart was not influenced by TM. ADP-induced aggregation of platelets was antagonized by TM. These data indicate that TM induced coronary dilation is partly due to a papaverine like action and also to ganglion-blocking, neuron-blocking and anti-adrenergic action. On the other hand, TM possessed catecholamine release and cardiotonic action as related to beta-receptors.
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PMID:[Pharmacology of cornary dilator agent, trapymin. (2) Analysis of its mode of action]. 124 70

Many reports indicate that serotonin plays a role in the regulation of the hypothalamo-pituitary-adrenocortical axis. The present study was designed to elucidate whether the activation of the central serotonergic pathway enhances adrenocorticotropin and corticosterone secretion, and if so, whether the CRH and vasopressin neuronal systems could be mediating this effect. Intraperitoneal administration of a low dose of L-5-hydroxytryptophan (an aromatic L-amino acid precursor of serotonin synthesis; 20 mg/kg bw, 30 minutes before the sacrifice) in rats pretreated with pargyline (a brain monoamine oxidase inhibitor, which enhances monoamine activity; 75 mg/Kg bw, 16 hours before the sacrifice) and carbidopa (a peripheral active inhibitor of the decarboxylation of aromatic L-amino acids, which would permit more monoamine precursor to be available to the brain; 50 mg/Kg bw, 90 minutes before the sacrifice) increased ACTH and corticosterone secretion in plasma. Such an effect was partially blocked by metergoline (a serotonin type-1 and-2 receptor blocker; 1 mg/Kg bw, 90 minutes before the sacrifice), but not by spiperone (a serotonin type-2 and dopamine receptor antagonist; 0.5 mg/Kg bw. 90 minutes before the sacrifice). The activation of the central serotonergic system enhanced the CRH content in the median eminence, whereas it decreased the content of this neuropeptide in the medial basal hypothalamus. These effects were fully abolished by metergoline, but not by spiperone pretreatment. The activation of the serotonergic pathway did not influence the vasopressinergic neuronal system. In vitro experiments using hypothalamic-median eminence fragments incubated with serotonin solutions indicate that this monoamine possesses a CRH releasing effect at concentrations of 1 microM or more.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Stimulation of the hypothalamo-pituitary-adrenocortical axis by the central serotonergic pathway: involvement of endogenous corticotropin-releasing hormone but not vasopressin. 165 12

Among the biochemical theories proposed for schizophrenia the best-founded appears to be the dopaminergic theory. Dopaminergic agonists exacerbate schizophrenic symptoms. Neuroleptics, which are the most effective drugs in schizophrenia, are dopaminergic-blocking agents. Other biochemical disorders have been demonstrated in some cases of schizophrenia but results are not always consonant. The presence of abnormal compounds, i.e. methylated derivatives or phenylethylamine, has often been mentioned. Several disorders of enzymes have also been reported, such as a defect in beta-dopamine hydroxylase or an abnormal activity of the MAO which metabolizes the indolamines and catecholamines. Disorders of the metabolism of noradrenaline and serotonin have also been suggested, mainly on experimental evidence. Other compounds have been incriminated, such as endorphins, gamma-aminobutyric acid, lysine-8 vasopressin or prostaglandins. The action of neuroleptics can be ascribed to dopaminergic respector blockade, as a safe approximation. However, the demonstration of several dopaminergic pathways and of several types of receptors makes the understanding of their mode of action all the more difficult that they interplay with many other neurotransmittors.
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PMID:[Biochemistry of schizophrenia and mechanism of action of neuroleptics]. 613 Jun 4

Many of the neurochemical changes associated with aging brain, particularly lower choline acetyltransferase and higher monoamine oxidase, occur with greater severity in senile dementia, Alzheimer's type (SDAT). These alterations correlate with neuropathologic indices, e.g., the number of senile plaques and tangles. Although many different treatment techniques have been used, most have been unsuccessful. No strong data have supported the use of stimulants, Gerovital H3, or hyperbaric oxygen. Among the vasodilators, cyclandelate and hydergine may be of value in some but not most patients. Much recent work has focused on techniques to increase acetylcholine brain concentrations. To date, precursors, such as choline, seem to have very limited value. Postsynaptic treatments, e.g., physostigmine, hold more hope for future benefit, if longer acting oral preparations are developed. Other compounds, such as ACTH, vasopressin, and piracetam, may have some value but need better definition and treatment indications. Recent discoveries on the influences of lecithin on membrane fluidity and receptor binding, may affect the focus of future pharmacologic investigation.
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PMID:Chemotherapy of cognitive disorders in geriatric subjects. 632 57

In the rat hypothalamus, antibodies to ovine CRF41 stain neurons of a paraventriculo-infundibular neuroglandular pathway. CRF like immunoreactivity (CLI)-containing perikarya are mostly packed in the parvocellular division of the paraventricular nucleus. Their morphology and topography differ from that of other peptidergic neurons. However a few CLI perikarya are also stained with vasopressin antibodies. CLI neurons project massively to the external layer of the median eminence (ELME). Adrenalectomy induced a total depletion of ELME CLI 12 to 24 h after surgery, followed by a secondary accumulation already conspicuous 5 days later. This biphasic evolution, identical to that of ELME vasopressin, is totally prevented by a replacement therapy with dexamethasone. Reserpine also induces an acute depletion of ELME CLI and vasopressin, that can be prevented by a monoamine oxidase inhibitor pretreatment. These results indicate the involvement of CLI neurons in the corticotropic axis, suggesting that they are indeed corticoliberin neurons. Among the extrahypothalamic locations of CLI neurons their abundance in the amygdala central nucleus is of interest since it is involved in the corticotropic axis. A similar pattern of CLI was noticed in several mammalian brains and also in lower vertebrates (birds, reptiles, amphibians, fishes). Species adaptations of CLI neurons were observed: CLI neurons are of the cerebrospinal fluid contacting type in the turtle. CLI fibres terminate close to corticotrophs in the fish pituitary. This suggests a direct excitosecretory role of CRF on these cells and concurs with a CRF function of CLI peptide even in fishes. CLI processes and terminals appear in the human fetal ELME at the 16th week of development and increase in number during the following weeks. Perikarya are seen at 19 weeks. In the rat CLI fibers and perikarya were detected as early as the 18th day of fetal development. Thus, paraventriculo-infundibular CLI system develops later than corticotrophs. This chronology perfectly concurs with the results of previous physiological and experimental studies.
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PMID:Corticoliberin neurons: cytophysiology, phylogeny and ontogeny. 636 84


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