Compensatory gastroprotective role of glucocorticoid hormones during inhibition of prostaglandin and nitric oxide production and desensitization of capsaicin-sensitive sensory neurons

被引:13
|
作者
Filaretova L. [1 ,2 ]
Bobryshev P. [1 ]
Bagaeva T. [1 ]
Podvigina T. [1 ]
Takeuchi K. [2 ]
机构
[1] Laboratory of Experimental Endocrinology, Pavlov Institute of Physiology, Russian Academy of Sciences, St. Petersburg 199034
[2] Department of Pharmacology and Experimental Therapeutics, Kyoto Pharmaceutical University, Misasagi, Yamashina
基金
俄罗斯基础研究基金会;
关键词
Capsaicin-sensitive sensory neurons; Gastric erosions; Gastroprotection; Glucocorticoid hormones; Indomethacin; Nitric oxide; Prostaglandins;
D O I
10.1007/s10787-007-1589-x
中图分类号
学科分类号
摘要
Glucocorticoid hormones produced in response to various ulcerogenic stimuli contribute to the maintenance of the gastric mucosal integrity. The role of glucocorticoids in gastroprotection becomes especially important where there is deficiency of prostaglandins (PGs) or nitric oxide (NO) or desensitization of capsaicin-sensitive sensory neurons (CSN). It has been found that neither inhibition of PG or NO production nor desensitization of CSN by itself provokes damage in the gastric mucosa of rats with normal corticosterone levels. However, each of these treatments results in mucosal damage in adrenalectomized rats; this effect being prevented by corticosterone replacement. Indomethacin-induced gastric erosions are potentiated to similar degrees by adrenalectomy, inhibition of NO production or desensitization of CSN. The potentiation caused by inhibition of NO production or CSN desensitization is further enhanced by concomitant glucocorticoid deficiency. These results suggest a pivotal compensatory role of glucocorticoids in the maintenance of the gastric mucosal integrity under the adverse conditions where the gastroprotective mechanisms provided by PGs, NO and capsaicin-sensitive sensory neurons are impaired. © 2007 Birkhäuser Verlag.
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页码:146 / 153
页数:7
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