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)

As part of a continuing investigation of the steric and electronic functions of the disulfide group in neurohypophyseal hormones on their biological activity, the synthesis of "oxytocin lactam", [cyclo-(1-aspartic acid,6-alpha,beta-diaminopropionic acid)]oxytocin, has been undertaken. The protected nonapeptide was prepared in a stepwise manner by solution techniques; after removal of side-chain protecting groups, formation of the briding amide bonds was accomplished by oxidation-reduction condensation. The analogue possesses rat uterotonic, avian vasodepressor, and rat antidiuretic potencies of 16 +/- 2, 6.6 +/- 0.6, and 5.6 +/- 3.8 units/mg, respectively.
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PMID:Replacement of the disulfide bond in oxytocin by an amide group. Synthesis and some biological properties of (cyclo-(1-L-aspartic acid,6-L-alpha,beta-diaminopropionic acid))oxytocin. 61 41

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.
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PMID:A1 neurons and excitatory amino acid receptors in rat caudal medulla mediate vagal excitation of supraoptic vasopressin cells. 145 Sep 50

The effects of N-methyl-D-aspartic acid (NMDA), injected s.c. or i.p. in the dose range of 2.5-10 mg/kg, on oxytocin and vasopressin levels were assessed in conscious rats. NMDA administration was found to induce a dose-related increase in oxytocin concentration with a peak response at 7.5 min. Plasma vasopressin was elevated only after injection of the highest dose used (10 mg/kg). Thus, though at different thresholds, the release of both posterior pituitary hormones was stimulated after NMDA administration.
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PMID:N-methyl-D-aspartic acid injected peripherally stimulates oxytocin and vasopressin release. 147 91

1. Recently it has been shown that injection of angiotensin II into the anterior diencephalon causes the rat to drink water. In the present experiments the dipsogenic action of a number of other substances including substances related to angiotensin was tested.2. Injection of 0.001 Goldblatt u. renin into the angiotensin-sensitive region causes the water-replete rat to drink. Drinking is slower in onset and continues for longer than after injection of angiotensin II.3. Synthetic tetradecapeptide renin substrate and angiotensin I were as effective as angiotensin II at causing water-replete rats to drink.4. beta-aspartic acid(1)-valine(5)-angiotensin II was also fully effective; but the D-arginine substituted octapeptide was much less effective.5. The (2-8) heptapeptide retained about 50% of the dipsogenic activity of the octapeptide, whereas the absence of phenylalanine at the other end of the peptide chain in the (1-7) heptapeptide results in an inactive compound.6. The (3-8) hexapeptide and the (4-8) pentapeptide, both of which have phenylalanine at the end of the chain, and the (1-4) and (5-8) tetrapeptide fragments of angiotensin II showed only a slight action on intake of water.7. Kallikrein, bradykinin, adenosine-3'5-cyclic phosphate, vasopressin and oxytocin caused no drinking when injected into the angiotensin-sensitive region.8. It is concluded that the requirements for the dipsogenic activity of angiotensin are the same as those for its other biological actions with the qualification that the precursor peptides are also active, presumably because they give rise to angiotensin II locally.
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PMID:The effect on drinking of peptide precursors and of shorter chain peptide fragments of angiotensin II injected into the rat's diencephalon. 432 62

The L-asparaginase activities of the brains of the Wistar, heterozygous and homozygous Brattleboro rats divided into three parts namely the anterior, middle and posterior which respectively contained cerebral cortex, hippocampus + midbrain + thalamus + hypothalamus cerebellum + pons + medulla oblongata were estimated. The L-asparaginase activities of all the three parts in the homozygous Brattleboro rats were significantly higher than in the Wistar rats as well as in the heterozygous Brattleboro rats. Twenty min following the injections of 200 mg/kg D-aspartic acid, 20 mg/kg morphine, 200 mg/kg D-aspartic acid + 20 mg/kg morphine, 6 mg/kg prolyl-leucyl-glycinamide (PLG) and 6 mg/kg PLG + 20 mg/kg morphine the L-asparaginase activities of all three parts of the homozygous Brattleboro rat brains were found to be significantly inhibited. After having seen the suppressive effect of the drugs and their combinations used before the homozygous Brattleboro rats were given D-aspartic acid, morphine, D-aspartic acid + morphine, PLG and PLG + morphine for seven days. Then their plasma vasopressin levels were determined by RIA. The treatments applied to the homozygous Brattleboro rats caused the appearance of a significant amount vasopressin in the plasma. The results were interpreted as evidence for the fact that the inhibition of the brain L-asparaginase provides and/or accelerates the biosynthesis and/or release of vasopressin. As morphine has a vasopressin releasing and a brain L-asparaginase inhibiting effect the antidiuretic action of morphine was considered to be linked to its inhibitory effect on the brain L-asparaginase.
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PMID:Vasopressin release by D-aspartic acid, morphine and prolyl-leucyl-glycinamide (PLG) in DI Brattleboro rats. 614 63

Application of information derived from a three-dimensional model of vasopressin bound to its antidiuretic receptor resulted in the design and synthesis of a bicyclic vasopressin analog, [5,8-cyclo(1-beta-mercaptopropionic acid,2-phenylalanine,5-aspartic acid,8-lysine)]vasopressin. The analog acts as an antagonist of the antidiuretic activity of vasopressin.
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PMID:A conformationally constrained vasopressin analog with antidiuretic antagonistic activity. 654 6

Studies were carried out on the right auricle of the right atrium of two-day-old rats placed in a special chamber perfused with Ringer-Locke solution at room temperature. The contractions rate of the auricle was counted with the use of a stereomicroscope. The following amino acids dissolved in Ringer-Locke solution were tested: glycine, glutamic acid, serine, alanine, aspartic acid, gamma aminobutyric acid, leucine, and peptides: vasopressin and oxytocin. Glutamic acid in a concentration of 10(-1) mol/l induced a decrease in auricle contraction rate by 25%. Alanine in concentration 10(-2) mol/l induced a decrease by 22%. Leucine in concentration 10(-2) mol/l induced a decrease by 16% and in concentration ten times higher a decrease by 28%. The other tested amino acids, vasopressin and oxytocin in concentration used had no influence on the rate of contraction frequency of the isolated auricle.
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PMID:The influence of amino acids, vasopressin and oxytocin on spontaneous contraction of the right auricle of the right atrium of two-day-old rats in vitro. 654 86

In chronically cannulated conscious chickens, Gallus gallus, native chicken angiotensin II ([Asp1,Val5]ANG II) caused biphasic blood pressure responses, a depressor followed by a pressor response. The pressor response appears to be mediated primarily by catecholamines. The depressor responses increased with increasing doses and were accompanied by tachycardia. The onset of the depressor action of [Asp1,Val5]ANG II (2.49 +/- 0.22 s) was nearly as quick as that of acetylcholine or histamine. Replacement of aspartic acid in position 1 with sarcosine or asparagine reduced both depressor and pressor potencies, whereas there was no difference either in depressor or pressor potencies between [Asp1,Val5] and [Asp1,Ile5]ANG II. The depressor response to [Asp1,Val5]ANG II was not inhibited by atropine, a vasopressin antagonist, prostaglandin synthetase inhibitors, methysergide, or propranolol but was blocked markedly by [Sar1, Ile8]ANG II and partially by [Sar1,Thr8]ANG II. The results suggest that the vasodepressor action of ANG II is mediated by angiotensin receptors and may possibly be a direct action on the vascular smooth muscle.
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PMID:Vasodepressor action of angiotensin in conscious chickens. 711 76

Bcl2 overexpression prevents axotomy-induced neuronal death of neonatal facial motoneurons, as defined by morphological criteria. However, the functional properties of these surviving lesioned transgenic neurons are unknown. Using transgenic mice overexpressing the protein Bcl2, we have investigated the bioelectrical properties of transgenic facial motoneurons from 7 to 20 days after neonatal unilateral axotomy using brain-stem slices and whole cell patch-clamp recording. Nonaxotomized facial motoneurons from wild-type and transgenic mice had similar properties; they had an input resistance of 38 +/- 6 M omega and fired repetitively after injection of positive current pulses. When cells were voltage-clamped at or near their resting membrane potential, alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), N-methyl-D-aspartic acid (NMDA), or vasopressin generated sustained inward currents. In transgenic axotomized mice, facial motoneurons could be found located ipsilaterally to the lesion; they had an input resistance of 150 +/- 30 M omega, indicating that they were smaller in size, fired repetitively, and were also responsive to AMPA, NMDA, and vasopressin. Morphological measurements achieved 1 week after the lesion have shown that application of brain-derived neurotrophic factor prevented the reduction in size of axotomized transgenic motoneurons. These data indicate that Bcl2 not only prevents morphological apoptotic death of axotomized neonatal transgenic motoneurons but also permits motoneurons to conserve functional electrophysiological properties.
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PMID:Axotomized neonatal motoneurons overexpressing the bcl2 proto-oncogene retain functional electrophysiological properties. 863 1

In order to evaluate the role played by vasopressin on pressor responses elicited by stimulation of the periaqueductal gray (PAG) area by excitatory amino acids we carried out in vivo studies in genetically vasopressin deficient rats (Brattleboro). Microinjections of 1-glutamic acid (glutamate, 0.6 to 60 nmol/rat) or N-methyl-d-aspartic acid (NMDA, 0.07 to 7 nmol/rat) into the PAG area of freely moving Brattleboro rats induced increases of arterial blood pressure values significantly lower than those obtained in Long Evans rats (control) (glutamate in Brattleboro rats: from +2+/-1 mmHg to 16+/-3 mmHg; glutamate in Long Evans rats: from +16+/-2 mmHg to +36+/-4 mmHg; NMDA in Brattleboro rats: from +5+/-2 mmHg to +34 +/-8 mmHg; NMDA in Long Evans rats: from +18+/-7 mmHg to 80+/-9 mmHg; n=5). Similarly, in anaesthetized Brattleboro rats (urethane 1.2 g/kg i.p.) pressor responses to NMDA microinjections (0.7 nmol/rat) into the PAG area were significantly lower than in Long Evans rats (controls) (+15+/-3 mmHg vs +24+/-4 mmHg). In Long Evans rats NMDA injection also reversed blood pressure decrease induced by ganglionic blocker, hexamethonium and/or losartan (3 mg/kg i.v.), an AT1 receptor antagonist. In Brattleboro rats, NMDA injection did not reverse blood pressure decreases induced by hexamethonium (5 mg/kg i.v.). Moreover, hexamethonium induced blood pressure decrease was not reversed by acetylcholine injection (137 nmol/rat) into the PAG area of anaesthetized Long Evans rats, but if injected before hexamethonium, acetylcholine was able to increase blood pressure (+25+/-3 mmHg). Our results document: i) the importance of the PAG area in the control of cardiovascular system; ii) the involvement of excitatory amino acids in the neural control of vasopressin release; iii) the close relationship between glutamate and vasopressin in the central blood pressure regulation.
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PMID:Role of vasopressin on excitatory amino acids mediated pressor responses in the periaqueductal gray area. 965 Aug 3


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