Calcium-mediated metabolic stimulation of neuroendocrine structures by intraventricular endothelin-1 in conscious rats
Autor: | Ben H. Chew, Donald F. Weaver, F.J. Espinosa, Paul M. Gross, Dan S. Wainman |
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Rok vydání: | 1993 |
Předmět: |
Male
medicine.medical_specialty Vasopressin Consciousness Stimulation Biology Rats Sprague-Dawley Pineal gland Endocrine Glands Internal medicine medicine Animals Molecular Biology Injections Intraventricular Circumventricular organs Endothelins General Neuroscience Brain Subfornical organ Rats Glucose medicine.anatomical_structure Endocrinology Hypothalamus Median eminence Autoradiography Calcium Nimodipine Neurology (clinical) Developmental Biology Endocrine gland |
Zdroj: | Brain Research. 606:135-142 |
ISSN: | 0006-8993 |
Popis: | We examined the hypothesis that the vascular- and brain-derived peptide, endothelin-1 (ET), would affect cerebral neuroendocrine structures when administered via the peripheral circulation or via a lateral cerebral ventricle (i.c.v.). ET was infused intravenously (14 nmol/min) or injected i.c.v. (9 pmol) in conscious rats in which local cerebral glucose metabolism was assessed by the quantitative autoradiographic [14C]deoxyglucose technique. Whereas intravenously infused ET was previously demonstrated to selectively stimulate metabolic activity in the pituitary intermediate and anterior lobes of conscious rats, it was without effect in 20 individual structures or subnuclei involved in neuroendocrine functions, including several circumventricular organs. Intraventricular ET, however, caused hypermetabolic responses in 9 neuroendocrine structures, including the pineal gland, subfornical organ, median eminence, the hypothalamic paraventricular and supraoptic nuclei, and other hypothalamic and preoptic structures. The metabolic stimulation resulting from central ET was abolished or attenuated regionally by i.c.v. pretreatment with the calcium L-channel inhibitor, nimodipine. The findings indicate that i.c.v. ET elicits a calcium-mediated hypermetabolic effect on several neuroendocrine structures in the forebrain involved in the regulation of fluid homeostasis, the cardiovascular system, and body temperature. |
Databáze: | OpenAIRE |
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