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 effects of postnatal methyl mercury exposure on the ontogeny of renal and hepatic responsiveness to trophic stimuli were examined. Increased ornithine decarboxylase (ODC) activity was used as an index of tissue stimulation. In the rat, renal ODC responsiveness to growth hormone, angiotensin, vasopressin, isoproterenol, and serotonin was absent at birth and matured 3 to 4 weeks later. However, pups exposed to methyl mercury showed marked, ODC responses to these same agents as early as 10 to 19 days of postnatal age, accompanied by a significant renal hypertrophy. In contrast to the kidney, the liver of normally developing rats was responsive to trophic factors even in the neonate. In this tissue, there was no consistent effect of neonatal methyl mercury treatment on ODC responses at any developmental stage tested; although absolute liver weights were reduced, liver/body weight ratio was not affected. These results demonstrate that postnatal methyl mercury exposure causes a precocious onset of ODC responses to trophic agents specifically in the kidney. Altered responsiveness may mediate some of the effects of this organomercurial on overall renal development and function.
 ...
PMID:Postnatal methyl mercury exposure: effects on ontogeny of renal and hepatic ornithine decarboxylase responses to trophic stimuli. 402 2

We have previously reported that maternal deprivation of rat pups causes a decrease in tissue responsiveness to growth hormone that is mediated by the loss of maternal tactile stimulation. We now report that liver responses to alpha and beta adrenergic agonists as well as glucagon and vasopressin decrease during maternal deprivation. However, the decreased responsiveness to these agents is mediated by short-term food deprivation (FD) rather than loss of maternal tactile stimulation. When 8-day-old rat pups were separated from the mother or placed with a nipple-ligated mother for 2 hr and then injected with phenylephrine, isoproterenol or glucagon, liver ornithine decarboxylase (ODC) activity did not increase, although ODC activity increased markedly in control pups after administration of these agents. This loss of responsiveness appears to be both tissue- and drug-specific, as liver ODC responses to dexamethasone, dibutyryl cyclic AMP and prostaglandin E-1 and heart ODC responses to phenylephrine were not affected. FD had only a slight effect on glycogen phosphorylase activation by phenylephrine and had no effect on phenylephrine-induced glycogen depletion. Finally, FD did not affect the number of alpha-1 or beta receptors in liver of rat pups. These findings suggest that short-term FD selectively decreases liver ODC responses to certain agonists including alpha and beta adrenergic agonists by postreceptor mechanisms.
 ...
PMID:Selective loss of ornithine decarboxylase response to adrenergic agonists and glucagon during food deprivation of neonatal rats. 613

Quiescent 3T3 cells can be stimulated to enter S by defined factors. When used in combination, three polypeptide hormones (EGF, vasopressin, and insulin), or a tumor promotor and insulin, are very effective in stimulating DNA synthesis. Like serum, the defined factors also stimulate deoxyglucose uptake and induce the synthesis of ornithine decarboxylase during G1. The second stage of deoxyglucose uptake and the induction of ornithine decarboxylase are protein synthesis-dependent events. When added with the growth factors, mouse interferon inhibits the synthesis of DNA and the induction of ornithine decarboxylase but has no effect on the uptake of deoxyglucose. Kinetic experiments comparing the effect of inhibitors of translation or transcription on induction of ornithine decarboxylase with the effect of interferon suggest that interferon may affect the synthesis of enzyme by inhibiting both transcription and translation of message. The findings provide further support for the proposition that interferon exerts a differential effect on mitogen-stimulated events events which are dependent on continuous protein synthesis.
 ...
PMID:Differential effect of interferon on DNA synthesis, 2-deoxyglucose uptake and ornithine decarboxylase activity in 3T3 cells stimulated by polypeptide growth factors and tumor promotors. 616 Jan 62

The effect of ovine growth hormone (GH) on kidney ornithine decarboxylase (ODC) was studied in newborn, preweanling and young adult rats. Basal kidney ODC activity was very low from 4 to 22 days after birth but rose 20-fold by day 25; it remained elevated through day 45. GH failed to stimulate ODC in the first two weeks after birth. GH did however stimulate ODC markedly from 20 through 45 days. Kidney ODC was stimulated in the neonate by vasopressin and by isoproterenol, but not by angiotensin II. Liver ODC remained relatively low and stable during development, and was responsive to GH at all ages studied. We conclude that a) the pattern of development of basal kidney ODC appears to be unique to this tissue and may be related to the postnatal maturation of renal morphology and/or function, b) neonatal kidney ODC is unresponsive to certain hormones but is not completely refractory to stimulation. These findings may have implications for the role of hormones in the maturation of the kidney and in the regulation of early renal function.
 ...
PMID:Maturation of growth hormone stimulation of kidney ornithine decarboxylase in the rat. 707 Feb 14

The potent tumour promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) acts synergistically with all known mitogens to induce DNA synthesis in 3T3 cells. In contrast, the neurohypophyseal hormone vasopressin, which is mitogenic for 3T3 cells, fails to synergize with TPA to stimulate DNA synthesis, ornithine decarboxylase activity or 2-deoxyglucose uptake. Thus TPA acts through a pathway which converges with that used by vasopressin, and at least some of its biological effects occur through mechanisms normally utilized by specific hormones.
 ...
PMID:Phorbol esters and vasopressin stimulate DNA synthesis by a common mechanism. 743 81

Peptic ulcer is a common disorder of gastrointestinal system and its pathogenesis is multifactorial, where smoking and nicotine have significant adverse effects. Smoking and chronic nicotine treatment stimulate basal acid output which is more pronounced in the smokers having duodenal ulcer. This increased gastric acid secretion is mediated through the stimulation of H2-receptor by histamine released after mast cell degranulation and due to the increase of the functional parietal cell volume or secretory capacity in smokers. Smoking and nicotine stimulate pepsinogen secretion also by increasing chief cell number or with an enhancement of their secretory capacity. Long-term nicotine treatment in rats also significantly decreases total mucus neck cell population and neck-cell mucus volume. Smoking also increases bile salt reflux rate and gastric bile salt concentration thereby increasing duodenogastric reflux that raises the risk of gastric ulcer in smokers. Smoking and nicotine not only induce ulceration, but they also potentiate ulceration caused by H. pylori, alcohol, nonsteroidal anti-inflammatory drugs or cold restrain stress. Polymorphonuclear neutrophils (PMN) play an important role in ulcerogenesis through oxidative damage of the mucosa by increasing the generation of reactive oxygen intermediates (ROI), which is potentiated by nicotine and smoking. Nicotine by a cAMP-protein kinase A signaling system elevates the endogenous vasopressin level, which plays an aggressive role in the development of gastroduodenal lesions. Smoking increases production of platelet activating factor (PAF) and endothelin, which are potent gastric ulcerogens. Cigarette smoking and nicotine reduce the level of circulating epidermal growth factor (EGF) and decrease the secretion of EGF from the salivary gland, which are necessary for gastric mucosal cell renewal. Nicotine also decreases prostaglandin generation in the gastric mucosa of smokers, thereby making the mucosa susceptible to ulceration. ROI generation and ROI-mediated gastric mucosal cell apoptosis are also considered to be important mechanism for aggravation of ulcer by cigarette smoke or nicotine. Both smoking and nicotine reduce angiogenesis in the gastric mucosa through inhibition of nitric oxide synthesis thereby arresting cell renewal process. Smoking or smoke extract impairs both spontaneous and drug-induced healing of ulcer. Smoke extract also inhibits gastric mucosal cell proliferation by reducing ornithine decarboxylase activity, which synthesises growth-promoting polyamines. It is concluded that gastric mucosal integrity is maintained by an interplay of some aggressive and defensive factors controlling apoptotic cell death and cell proliferation and smoking potentiates ulcer by disturbing this balance.
 ...
PMID:Smoking and the pathogenesis of gastroduodenal ulcer--recent mechanistic update. 1461 84


<< Previous 1 2