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)

Discrete brain structures were analysed for gamma-aminobutyric acid (GABA) and vasopressin content in normo- and hypotensive rats treated with the glutamic acid decarboxylase inhibitor, 3-mercaptopropionic acid (MPA) and the GABAA agonist muscimol. In the normotensive group treated with MPA only, the concentration of vasopressin increased in the supraoptic nucleus, indicating an inhibitory role for GABA. In the hypotensive group a rise in the vasopressin level in the nucleus of the solitary tract was detected and the GABA level decreased in the supraoptic nucleus. Muscimol decreased the concentration of vasopressin in the nucleus of the solitary tract. The changes in the concentration of vasopressin may be a result of increased or decreased activation of the GABAergic system. The results show that the GABA- and vasopressinergic systems somehow interact although the more precise way of action remains to be clarified.
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PMID:Biochemical evidence for the GABA regulation of vasopressin levels in microdissected brain structures after servo-controlled hypotension. 278 40

The effects of specific treatments of the caudal ventrolateral medulla (CVLM) on vasopressin (AVP) release and arterial pressure (AP) were examined in urethane-anesthetized rabbits. Electrical stimulation of the CVLM for 5 minutes did not increase plasma AVP; it did however elicit an acute fall in arterial pressure. Similarly, stimulation of cells in the CVLM by microinjection of L-glutamate caused an acute decrease in AP but no change in plasma AVP. Muscimol injected into the CVLM increased AP but not AVP. On the other hand, bicuculline decreased AP and markedly increased plasma AVP, and the increase in AVP following bicuculline injection was not secondary to the fall in AP. These results demonstrate that the CVLM is involved in the regulation of AVP release. Furthermore, taken together with previous findings, these studies indicate that AVP and AP respond differently to treatments of the CVLM, suggesting that different cells in the CVLM are involved in the regulation of AVP release and AP.
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PMID:Caudal ventrolateral medulla can alter vasopressin and arterial pressure. 399 65

The A 1 noradrenergic neurones are known to project from the caudal ventrolateral medulla to the vasopressin-secreting neuroendocrine cells in the hypothalamus. They therefore represent a possible central pathway from the medulla to the hypothalamus for baroreceptor-initiated secretion of vasopressin. We tested this hypothesis in the anaesthetized rabbit. Muscimol, a gamma-aminobutyric-acid-receptor agonist, was injected into the caudal ventrolateral medulla to inhibit the A 1 noradrenergic neurones. Secretion of vasopressin, measured by radioimmunoassay, was initiated either by arterial haemorrhage or by constriction of the inferior vena cava. After injection of vehicle into the caudal ventrolateral medulla, or after injection of muscimol into nearby control areas, both haemorrhage and constriction of the inferior vena cava produced the expected elevation in plasma vasopressin. After injection of muscimol into the caudal ventrolateral medulla, secretion of vasopressin in response to haemorrhage and to constriction of the inferior vena cava, was completely abolished. The A 1 noradrenergic neurones may be the sole pathway transmitting the reflex for baroreceptor-initiated secretion of vasopressin from the medulla to the hypothalamus.
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PMID:Inhibiting the rabbit caudal ventrolateral medulla prevents baroreceptor-initiated secretion of vasopressin. 405 99

Vasopressin-containing neurosecretory cells are partly regulated by GABAergic neurons present both at the hypothalamic and the pituitary level. In the present work, we compared GABA effects on vasopressin release from posterior pituitaries of Sprague-Dawley (SPD), Wistar (W), Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Release of vasopressin was studied in vitro by placing neurointermediate lobes in perfusion chambers. It was stimulated twice by 50 mM KCl (S1 and S2) and the ratio between the first and the second stimulation was calculated (S2/S1). The basal and stimulated release of vasopressin was enhanced in the SHR. There was no difference in vasopressin content in the pituitary between the WKY and the SHR but the levels were lower compared to the SPD rat. Muscimol, a GABA-A receptor agonist, was added during S2. Muscimol inhibited in a dose-dependent manner the stimulated release of vasopressin, with an ED50 about 3 microM. The effect of muscimol was not statistically different between the strains expressed in ratios. The actual inhibition was apparently greater in the SHR, as both basal and stimulated vasopressin release was larger.
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PMID:GABA-A agonist muscimol inhibits stimulated vasopressin release in the posterior pituitary of Sprague-Dawley, Wistar, Wistar-Kyoto and spontaneously hypertensive rats. 811 20

gamma-Aminobutyric acid (GABA) is contained in many neurons in the suprachiasmatic nucleus (SCN), and is considered to be a circadian entraining factor. Arg-vasopressin (AVP)-containing neurons represent one of the output paths from the SCN to other brain areas. We examined the effects of GABA, muscimol (GABA-A agonist), bicuculline (GABA-A antagonist), baclofen (GABA-B agonist) and phaclofen (GABA-B antagonist) on AVP release using SCN slice preparations in culture. SCN slices were prepared from coronally sliced brain tissue and cultured in organic tissue culture dishes with DMEM/N2 medium in a CO2 (5%) incubator. The culture medium was changed at 3-h intervals until 9 h after 3 h application of each drug. Concentrations of AVP in 1 ml aspirates of the medium were analyzed by EIA. Muscimol (1, 10 microM) increased and bicuculline (1, 10, 100 microM) decreased the AVP release 3-6 h after application. However, baclofen and phaclofen had no apparent effects on AVP release. Riluzole (0.1 mM) and nipecotic acid (1 mM), GABA uptake inhibitors, increased AVP release 3-6 h after application. These results indicate that GABA promotes AVP release mediated by GABA-A receptors in the SCN.
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PMID:GABAergic control of Arg-vasopressin release from suprachiasmatic nucleus slice culture. 917 89