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)

Aggressive treatment with H(2) receptor blocking agents and/or antacids has been advocated as effective prophylaxis against and treatment for "stress ulcer," based on the logical but infrequently tested assumption that the severity of the disease is critically determined by the concentration of intraluminal acid. The present study investigated this assumption in a model which employed topical acid, topical bile acid and mucosal ischemia to induce ulcerogenesis. With vascularized, chambered ex vivo wedges of canine proximal gastric wall, groups of animals were studied during three sequential periods using topical test solutions (TS) containing either 0 mM, 100 mM or 160 mM HCI. During period 1, mucosae were exposed to TS alone; during period 2, either to TS containing 1 mM sodium taurocholate (TC) or to TS and concomitant vasopressin infusion (VP); and during period 3, to TS + TC + VP. Parameters evaluated included net H(+) flux ( big up tri, openH(+)), aminopyrine clearance (AC), a measure of mucosal blood flow, net TC flux ( big up tri, openTC) and the lesion index, graded 0-5. The data indicate that in nonischemic mucosa exposed to constant [TC], AC was significantly increased, big up tri, openH(+) ("back-diffusion") increased as a linear function of [H(+)] and no lesions were observed. Under the same circumstances in ischemic mucosa, big up tri, openH(+) increased as linear function of [H(+)]. As a consequence, lesion severity was also a linear function of [H(+)]. big up tri, openTC was enhanced at low pH but bore no relation to the degree of mucosal damage induced. Assuming applicability of the model, these studies provide support for the use of H(2) receptor blocking agents and/or antacids to prevent or ameliorate "stress ulcer" disease.
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PMID:Influence of hydrogen ion concentration on bile acid induced acute gastric mucosal ulcerogenesis. 3 49

Influences of restraint plus water-immersion stress on gastric alkaline response and mucosal blood flow were investigated in the rat. Under normal conditions, the stomach secreted alkali at the rate of approximately 1 microEq/15 min in the presence of omeprazole (60 mg/kg i.p.) and responded to mucosal acidification (1000 mM HCI for 10 min) by a significant rise of output (approximately 2.5 microEq/15 min), and the latter process was significantly blocked by indomethacin (5 mg/kg s.c.), quinacrine (100 mg/kg s.c.) and vasopressin (10 unit/kg/hr i.v.). Restraint alone decreased basal rates of HCO3- secretion but had no effect on acid-induced HCO3- output. Additional water-immersion stress further reduced alkaline secretion, totally abolished the increased HCO3- response to acid and significantly suppressed the increase of HCO3- output caused by 16,16-dimethyl prostaglandin E2 (3-30 micrograms/kg s.c.). During restraint stress mucosal blood flow was reduced only by 30% but after exposure to additional water-immersion, it further decreased to about 25% of normal values. Both indomethacin and quinacrine had no effect on mucosal blood flow, whereas vasopressin markedly reduced mucosal blood flow by about 80%. These results suggest that stress not only reduced basal rates of alkaline secretion in the stomach but also impaired the mucosal ability to increase HCO3- output in response to acid. These secretory disorders caused by stress may be attributed to both a decrease of mucosal blood flow and prostaglandin deficiency in the mucosa.
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PMID:Influences of stress on gastric alkaline secretion in rats. 231 69

Hypothalamic median eminence extracts (MEE) were subjected to gel filtration on Sephadex G-25 and G-75 columns to characterize the corticotropin releasing factor (CRF) in relation to arginine vasopressin (AVP). CRF activity was measured using monolayer cultured anterior pituitary cells, and AVP was measured by radioimmunoassay. Sephadex G-25 chromatography of AVP immunoreactivity of MEE (NIAMDD-Rat HE-RP-1) showed three peaks on elution with 0.1 N HCI and four peaks on elution with 0.2M acetic acid. But freshly prepared MEE showed only one peak on elution with 0.1 N HCI. These results suggest that AVP in NIAMDD-Rat HE-RP-1 is polymerized or aggregated on the Sephadex G-25 column, especially when eluted in 0.2M acetic acid. Two main peaks of CRF activity appeared consistently on both Sephadex G-25 and G-75 chromatography. One was near the void volume and the other was retarded. The small molecular CRF (small-CRF) peak was coeluted with immunoreactive AVP and 125I-AVP, on both chromatographies on elution with 0.1 N HCI. The large molecular CRF (big-CRF) appeared between the void volume and I-39 ACTH on Sephadex G-75 chromatography. Big-CRF from freshly prepared MEE had no AVP immunoreactivity. AVP showed CRF activity in pituitary cell cultures, but its CRF activity accounted for no more than 20% of the CRF activity of NIAMDD-Rat HE-RP-1. The log dose-response characteristics of the CRF activities of small-CRF and AVP differed. These results suggest that the median eminence has at least two substances with CRF activity: one is large molecular CRF, and the other is small molecular CRF which may have a vasopressin-like molecular weight. AVP may account for a part of the CRF activity of small molecular CRF but is not identical with genuine CRF.
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PMID:Characterization of corticotropin releasing factor (CRF) and arginine vasopressin in median eminence extracts on sephadex gel-filtration. 697 67