Mechanisms underlying intracisternal TRH-induced stimulation of gastric acid secretion in rats |
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| Authors: | Y Taché Y Goto D Hamel A Pekary D Novin |
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| Institution: | 1. Center for Ulcer Research and Education, University of California, Los Angeles, CA 90024, U.S.A.;2. Endocrinology Research Laboratory, Veterans Administration Wadsworth Medical Center, University of California, Los Angeles, CA 90024, U.S.A.;1. Department of Medicine, Brain Research Institute, University of California, Los Angeles, CA 90024, U.S.A.;3. Department of Psychology, Brain Research Institute, University of California, Los Angeles, CA 90024, U.S.A. |
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| Abstract: | The neurohumoral pathways mediating intracisternal TRH-induced stimulation of gastric acid secretion were investigated. In urethane-anesthetized rats, with gastric and intrajugular cannulas, TRH or the analog N-Val2]-TRH (1 microgram) injected intracisternally increased gastric acid output for 90 min. Serum gastrin levels were not elevated significantly. Under these conditions the TRH analog, unlike TRH, was devoid of thyrotropin-releasing activity as measured by serum TSH levels. In pylorus-ligated rats, gastrin values were not modified 2 h after peptide injection whereas gastric acid output was enhanced. TRH (0.1-1 micrograms) stimulated vagal efferent discharge, recorded from a multifiber preparation of the cervical vagus in urethane-anesthetized rats and the response was dose-dependent. The time course of vagal activation was well correlated with the time profile of gastric stimulation measured every 2 min. These results demonstrated that gastric acid secretory stimulation elicited by intracisternal TRH is not related to changes in circulating levels of gastrin or TSH but is mediated by the activation of efferent vagal pathways that stimulated parietal cell secretion. |
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| Keywords: | vagal outflow gastrin TSH gastric acid secretion TRH TRH analog |
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