Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
 ...
PMID:The action of psychotropic drugs on DOPA induced behavioural responses in mice. 1 9

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.
 ...
PMID:[The hypothalamo-neurohypophysial system and antidiuretic hormone (author's transl)]. 33 45

1 In cats anaesthetized with chloralose, the central excitatory substances, tubocurarine, picrotoxin, bicuculline, leptazol and strychnine, were applied to the exposed ventral surface of the brain stem through paired Perspex rings placed across the medulla and their effects on vasopressin release and arterial blood pressure were examined.2 The excitatory substances released large amounts of vasopressin when applied to an area 6-9 mm caudal to the trapezoid bodies. From this area vasopressin release was previously obtained with nicotine.3 With nicotine, the vasopressin release occurred almost instantaneously and tachyphylaxis developed rapidly. With the excitatory substances the release increased gradually and there was no tachyphylaxis. When these substances were applied for several minutes, the release reached its maximum a considerable time after their removal, except with leptazol when release diminished at once after removal.4 The excitatory substances had little or no effect on arterial blood pressure when applied to the vasopressin releasing area, but produced strong pressor responses when applied to a more rostrally situated area.5 It is concluded that the excitatory substances release vasopressin and raise arterial blood pressure because they are antagonists of gamma-aminobutyric acid and/or glycine and that numerous inhibitory neurones which release these amino-acids synapse at the ventral surface of the medulla. The physiological function of those which synapse at the vasopressin releasing area may be to act as a brake on vasopressin release, and of those which synapse at the more rostrally situated area to act as a brake on arterial blood pressure.
 ...
PMID:Vasopressin release produced in anaesthetized cats by antagonists of gamma-aminobutyric acid and glycine. 62 Jan 1

(1) The effects of 5 anesthetics (chloralose, chloroform, ethanol, pentobarbital and urethane) and one anticonvulsant (diphenylhydantoin) were studied on the membrane properties and post-synaptic responses of crustacean neuromuscular junction preparations and molluscan neurons to putative transmitters and peptides. (2) In crustacean preparations pentobarbital selectively depressed, in a dose-dependent, reversible manner, post-synaptic, Na+-dependent, depolarizing responses to the putative transmitter glutamate without altering post-synaptic, Cl(-)-dependent inhibitory responses to the putative transmitter gamma-aminobutyric acid. (3) The effects of all the agents on post-synaptic pharmacology of a molluscan neurosecretory cell were studied either by causing the cell to hyperpolarize to about--100mV through repeated application of acetylcholine (ACh) in a K+-free, Ca++-containing solution or by hyperpolarization through injection of intracellular current in a K+-free solution. Effects of these agents on post-synaptic responses on other molluscan neurons were studied using intracellular current injection to manipulate membrane potential. (4) All of the agents tested selectively depressed the depolarizing Na+-K+-dependent post-synaptic responses of the neurosecretory cell to ACh in a dose-dependent reversible manner without appreciably altering the membrane properties of the cell (over the potential range of the ACh responses). (5) Pentobarbital did not alter the inversion potential of the ACh response. (6) Reciprocal plot analysis of all of the agents tested revealed that the antagonism of the ACh response was primarily non-competitive. (7) None of the agents tested altered hyperpolarizing, K+-dependent responses to dopamine and glutamate on the neurosecretory cell, nor did they affect either the induction or enhancement of BPP activity by the vertebrate peptide vasopressin on this cell.
 ...
PMID:CNS depressants: effects on post-synaptic pharmacology. 117 46

Extracellular recordings from the supraoptic nucleus of the rat established that vasopressinergic neurosecretory cells were excited by stimulation of cervical but not abdominal vagal afferents. This response was absent or significantly attenuated after microinjection of gamma-aminobutyric acid into a region of the caudal medulla known to contain the A1 noradrenaline cell group. Consistent with the possible involvement of the A1 group, vagal stimulation approximately doubled the frequency of proto-oncogene expression in A1 noradrenaline neurons, as indicated by the occurrence of nuclear Fos-like immunoreactivity in tyrosine hydroxylase-positive neurons of the caudal ventrolateral medulla. Finally, A1 region microinjection of either the N-methyl-D-aspartic acid (NMDA) receptor antagonist DL-2-amino-5-phosphonovaleric acid (APV), or the non-NMDA antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), significantly reduced vasopressin cell responses to vagal stimulation. These findings suggest that: (i) the A1 group is an essential component in a pathway which relays facilitatory vagal input of cardiopulmonary origin to neurosecretory vasopressin cells, and (ii) the activation of A1 neurons in this pathway involves both NMDA and non-NMDA excitatory amino acid receptors, an observation consistent with an input to A1 cells which generates 'mixed' excitatory postsynaptic potentials.
 ...
PMID:A1 neurons and excitatory amino acid receptors in rat caudal medulla mediate vagal excitation of supraoptic vasopressin cells. 145 Sep 50

The active immunization of rabbits and white rats to antidepressant sydnophen results in the formation of antibodies binding norepinephrine, dophamine, serotonine as well peptide regulatory compounds: substance P, pynorphine, vasopressin and beta-endorphin. The immunization against endogenic antidepressant thyroliberin induces the formation of antibodies to the same biogenic amines and to the gamma-aminobutyric acid, oxytocin and leu encephalin. The data obtained are discussed in connection with some physiological and biochemical changes found earlier during immunization to antidepressants.
 ...
PMID:[Active immunization to exogenous and endogenous antidepressants. The formation of antibodies to biogenic amines and peptide regulators]. 205 18

This investigation tested the hypotheses that picrotoxin, a drug which blocks the inhibitory effect of gamma-aminobutyric acid (GABA), would, in spinal cord-transected rats, (1) suppress the cardiac vagus when localized to the forebrain and stimulate the cardiac vagus by acting in the brainstem and (2) stimulate the release of vasopressin into the systemic circulation through separate forebrain and brainstem GABAergic mechanisms. An intra-arterial infusion technique allowed for delivery of picrotoxin selectively to either forebrain or brainstem areas. Administration of picrotoxin via the vertebral artery decreased sinus rate and increased circulating levels of vasopressin. Infusion of picrotoxin into the internal carotid artery caused increases in sinus rate, blood pressure and plasma vasopressin. These data support the hypothesis that GABAergic mechanisms at different levels of the neuraxis exert opposite effects on cardiac vagal activity, and that GABAergic mechanisms in both the brainstem and forebrain inhibit the release of AVP into the systemic circulation.
 ...
PMID:Resolution of central sites involved in picrotoxin-induced vagal activation and vasopressin release. 216 74

We studied the effects of microwave irradiation during the incubation of free-floating brain sections with primary antibodies against gamma-aminobutyric acid (GABA), enkephalin and vasopressin. Vibratome sections of perfusion-fixed rat brain were incubated: (a) overnight at room temperature (20-22 degrees C), (b) during various periods of time under microwave irradiation, such that the induced temperatures did not exceed 10 degrees C, (c) same as (b) but with induced temperatures not exceeding 40 degrees C, (d) without microwave irradiation, at 4-10 degrees C (temperature control for (b)), (e) same as (d) but at 40 degrees C (temperature control for (c)). During the incubation-irradiation we continuously monitored the temperature and controlled it by cooling and by manipulating the energy output of the magnetron. The peroxidase immunocytochemical procedure was completed using for all sections the same incubation parameters. Selected GABA-immunoreacted sections were examined in the electron microscope. Incubation at 10 degrees C in the primary antiserum as short as 30 min, with or without microwave irradiation, already results in (weak) binding of the antibodies to immunoreactive structures. One or 2 h of incubation in the primary antiserum in the microwave oven at 40 degrees C or at the same temperature outside the microwave oven results in excellent staining of GABA-immunoreactive structures and of good staining of enkephalin- or vasopressin-immunoreactive structures. The ultrastructural details were much better preserved in incubated-irradiated sections than in sections incubated overnight and only slightly less preserved than in the other control sections. There is no improved penetration of the antibodies into the sections. We conclude that by using microwave technology or by raising the temperature of the incubation medium, the time of incubation, at least in these antisera, can be shortened drastically, whereas the ultrastructural details remain well preserved.
 ...
PMID:Immunocytochemistry on free-floating sections of rat brain using microwave irradiation during the incubation in the primary antiserum: light and electron microscopy. 228 84

1. In water-loaded rats under ethanol anaesthesia, the injection of 2-4 microliters 1.54M NaCl solution (hypertonic saline:HS) into a lateral cerebral ventricle (i.c.v.) produced an antidiuretic and a pressor response, together with increased urinary excretion of vasopressin and 'oxytocin-like radioimmunoreactivity' (OLRI). In lactating rats HS also produced a milk-ejection response which was shown to be due to the release of oxytocin. 2. The injection of 20-40 micrograms gamma-aminobutyric acid (GABA) or 40-80 ng muscimol i.c.v. 2 min before HS inhibited the antidiuretic, pressor and milk-ejection responses and reduced the urinary excretion of vasopressin and OLRI. 3. The pressor response to HS was abolished by a ganglion blocking agent but it was not reduced by a vasopressin antagonist. After the antagonist, the antidiuretic response to HS was abolished and the pressor response was accompanied by a diuresis both of which were blocked by muscimol. 4. The threshold dose of HS for an antidiuretic response was 4-8 times higher on injection into the cisterna magna (i.cist.) than when injected i.c.v. GABA, i.v. or i.cist, did not inhibit the response to HS i.c.v. 5. The results confirm other evidence that, in the rat, in contrast some other species, an osmotic stimulus causes release of both vasopressin and oxytocin. This release is blocked by GABA and muscimol. These drugs and HS act at a site reached not from the subarachnoid space but from the cerebral ventricles, probably the hypothalamus. The pressor response to HS under the experimental conditions used is due entirely to central sympathetic stimulation and this effect, as well as the release of vasopressin and oxytocin, is blocked by muscimol.
 ...
PMID:Central inhibition by gamma-aminobutyric acid and muscimol of the release of vasopressin and oxytocin by an osmotic stimulus in the rat. 233 82

Activation of nociceptive somatic afferents excites hypothalamic neurosecretory cells and stimulates the release of vasopressin. To investigate the possibility that relevant afferent information is relayed through the A1 norepinephrine cell group of the caudal ventrolateral medulla, single-unit recording experiments were performed in pentobarbital sodium-anesthetized rats. The effects of somatic nerve stimulation, application of noxious somatic stimuli, and A1 region stimulation on the activity of putative vasopressin-secreting neurosecretory cells of the supraoptic nucleus were compared. The predominant effect of femoral and sciatic nerve stimulation on these cells was excitation, 54% (n tested = 113) displaying a marked increase in discharge probability, which had a mean onset latency of 72 +/- 3 ms and a mean duration of 114 +/- 9 ms. Almost all cells (96%) responding to somatic nerve stimulation were also excited by pinching of the ipsilateral or contralateral hindlimb paw, and the majority (84%) displayed a matching but shorter latency response to A1 region stimulation (mean onset 35 +/- 4 ms, duration 55 +/- 9 ms). A1 region injections of the inhibitory neurotransmitter gamma-aminobutyric acid reversibly blocked the effects of both somatic nerve stimulation (n = 14) and paw pinch (n = 9) on putative vasopressin cells. These results indicate that excitation of vasopressinergic neurosecretory cells by noxious somatic stimuli requires activation of neurons of the caudal ventrolateral medulla and hence are consistent with the proposal of a role for the A1 norepinephrine cell group.
 ...
PMID:Noxious somatic stimuli excite neurosecretory vasopressin cells via A1 cell group. 236 Jun 97


1 2 3 4 5 6 7 8 Next >>