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)

The effect that several substances may have on ANF release by atrial slices and on its tissular content was investigated. alpha- and beta-adrenergic and cholinergic agonists, vasopressin, met-enkephaline, dexamethasone and DOC, in concentration ranging from 10(-4) to 10(-8) M, were added into the incubation media and incubated 1 and 4 hours. No changes were observed in ANF concentration either in the media or in its tissular concentration as measured by a specific radioimmunoassay. When intact rats were previously treated with DEXA, DOC or DEXA + DOC and their atria incubated "in vitro", an increase in the release of ANF was observed in the Dexa-treated group only, but all treated groups had higher tissular ANF concentration. It is concluded that neither alpha- or beta-adrenergic, nor cholinergic agonists or vasopressin and met-enkephaline stimulate ANF release "in vitro". On the other hand steroids may regulate ANF release and synthesis in the intact rat. It seems likely that the ANF released into the media corresponds to a short peptide.
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PMID:Mechanisms of release of atrial natriuretic factor. I. Effect of several agonists and steroids on its release by atrial minces. 293 80

We recently reported that ovine corticotropin releasing factor (CRF) infusion in conscious dogs elevated plasma vasopressin. The present study examines the vasopressin, adrenocorticotropic hormone (ACTH), and cortisol responses to CRF infusion (20 ng X kg-1 X min-1), to hypertonic saline infusion (NaCl 0.054 meq X kg-1 X min-1), and to simultaneous coinfusion of CRF and NaCl (CRF + NaCl) without (no-dex) or with (dex-treated) dexamethasone pretreatment in six conscious dogs (6-8 experiments/dog). CRF had no significant effect on plasma sodium or osmolality, blood pressure, or heart rate. NaCl increased plasma sodium from 146 +/- 1 to 151 +/- 1 meq/l and plasma osmolality from 298 +/- 3 to 305 +/- 3 mosmol/kg. Vasopressin increased significantly during CRF (2.1 +/- 0.5 to 4.8 +/- 1.1 pg/ml) and NaCl (1.9 +/- 0.3 to 5.0 +/- 0.8 pg/ml). Coinfusion of CRF and NaCl resulted in a response larger than the sum of the two infusions alone (3.0 +/- 1.6 to 31.4 +/- 18.5 pg/ml). The ACTH response to CRF (45 +/- 8 to 288 +/- 88 pg/ml) was not augmented by coinfusion with NaCl. DEX attenuated the vasopressin and ACTH responses to each infusion. We conclude that CRF-induced increases in vasopressin are augmented by a simultaneous osmotic stimulus. In addition, the plasma vasopressin responses to CRF and/or hypertonic saline infusion are inhibited by glucocorticoid pretreatment.
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PMID:Vasopressin responses to corticotropin releasing factor and hyperosmolality in conscious dogs. 302 13

The separate role of mineralocorticoid and glucocorticoid hormone action in maintaining arterial pressure was studied in normotensive rats. Four groups were prepared: adrenalectomized (ADX) rats given 6 micrograms aldosterone/24 h (ALDO; n = 9) or 10 micrograms dexamethasone/24 h (DEX; n = 9) by intraperitoneal Alzet pumps, shamoperated controls (control; n = 10) and ADX rats with no hormone replacement (ADX; n = 9). All groups were given 1% NaCl + 2.5% glucose drinking solution. Measurements of plasma corticosterone and aldosterone and urinary aldosterone excretion confirmed the adequacy of the experimental groups. Forty-eight hours after ADX or sham, base-line intra-arterial mean arterial pressure (MAP) in conscious undisturbed rats was similar in the four groups. Captopril (1 mg/kg iv) produced a similar reduction in MAP in ALDO (-11 +/- 2 mmHg) and DEX (-12 +/- 1 mmHg) groups, despite a lower plasma renin activity (PRA) in ALDO (2.0 +/- 0.7 and 6.0 +/- 1.5 ng X ml-1 X h-1, respectively; P less than 0.05). dP (Me)TyrAVP (50 micrograms/kg iv) caused a greater decrease in MAP in ALDO (-15 +/- 3 mmHg) than in DEX (-8 +/- 1 mmHg; P less than 0.05). Combined blockade with both antagonists resulted in a greater MAP reduction in ALDO (-29 +/- 4 mmHg) than in DEX (-15 +/- 4 mmHg; P less than 0.05). These results indicate that glucocorticoid hormone action maintains arterial pressure in ADX rats by mechanisms similar to normal rats and largely independent of the renin-angiotensin system and vasopressin. In contrast, mineralocorticoid replacement alone in ADX rats requires increased participation of both peptide systems for maintenance of arterial pressure.
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PMID:Role of mineralocorticoids and glucocorticoids in blood pressure regulation in normotensive rats. 353 7

Transient exposure of rats to high doses of dexamethasone (DEX; 500 microg/day for 5 days) produced a host of symptoms that are indicative of hypothalamic-pituitary-adrenal (HPA) axis dysregulation, such as increased adrenocortical secretion over 24 h, blunted and prolonged secretory response to emotional stress, refractoriness of adrenocorticotropin in vitro release to stimulation with the secretagogues corticotropin-releasing hormone (CRH) and vasopressin, decreased levels of mRNA encoding type II corticosteroid receptors in the hippocampus and increased numbers of transcripts encoding CRH in the paraventricular nucleus. Daily administration of melatonin (MEL; 80 microg/kg) concomitantly with, and for 5 days after discontinuation of, glucocorticoid treatment 'normalized' most of the symptoms of impaired HPA regulation caused by the exposure to DEX. While none of the treatments used caused major shifts in circadian patterns of corticosterone secretion, MEL administration was associated with diminished overall corticosterone secretion and increased sensitivity to glucocorticoid feedback. Taken together, these findings indicate that chronic MEL treatment may protect several regulatory components of the HPA axis from glucocorticoid-induced deterioration.
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PMID:Chronic melatonin treatment counteracts glucocorticoid-induced dysregulation of the hypothalamic-pituitary-adrenal axis in the rat. 963 Apr 34

Heme oxygenase (HO), the main enzyme deputed to heme metabolism, has been identified as two main isoforms called HO-1 and HO-2. HO-1 is inducible and plays a main role in the cellular oxidant/antioxidant balance whereas HO-2 is constitutive and involved in the physiological metabolism of heme. However, it is noteworthy to mention that HO contribute to the regulation of the hypothalamic release of neuropeptides such as corticotrophin-releasing hormone and arginine-vasopressin and could modulate the pulsatile release of gonadotropin releasing hormone (GnRH). GT1-7 cells are immortalized hypothalamic neurons and a valuable tool to evaluate hypothalamic neuroendocrine control of reproduction. The aim of this work was to investigate and characterize the presence of HO isoforms in the GT1-7 hypothalamic neurons. Hemin, a well-known inducer of HO-1, significantly increased HO activity, whereas dexamethasone did not modify HO-2 activity. Moreover, hemin and DEX, in combination, did not have any additive effect on HO activity in GT1-7 neurons. Furthermore, basal HO-1 immunoreactivity identified in GT1-7 cells, was significantly up-regulated by hemin. Conversely, no HO-2 immunoreactivity was detected. Taken together, these results suggest the presence of functional HO-1 in GT1-7 immortalized hypothalamic neurons and open new avenues about the use of this cell line for the study of HO modulation of GnRH secretion and reproduction.
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PMID:Heme oxygenase expression and activity in immortalized hypothalamic neurons GT1-7. 1870 74