PVN lesions prevent the endothelin 1-induced increase in arterial pressure and vasopressin
Departments of Medicine and Physiology, Wayne State University School of Medicine and John D. Dingell Veterans Affairs Medical Center, Detroit, Michigan 48201 Endothelin (ET) acts within the central nervous system to increase arterial pressure and arginine vasopressin (AVP) secretion. This study ass...
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Veröffentlicht in: | American journal of physiology: endocrinology and metabolism 2001-02, Vol.280 (2), p.E349-E356 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | Departments of Medicine and Physiology, Wayne State University
School of Medicine and John D. Dingell Veterans Affairs Medical
Center, Detroit, Michigan 48201
Endothelin (ET) acts within the
central nervous system to increase arterial pressure and arginine
vasopressin (AVP) secretion. This study assessed the role of the
paraventricular nuclei (PVN) in these actions. Intracerebroventricular
ET-1 (10 pmol) or the ET A antagonist BQ-123 (40 nmol) was
administered in conscious intact or sinoaortic-denervated (SAD)
Long-Evans rats with sham or bilateral electrolytic lesions of the
magnocellular region of the PVN. Baseline values did not differ among
groups, and artificial cerebrospinal fluid (CSF) induced no significant
changes. In sham-lesioned rats, ET-1 increased mean arterial pressure
(MAP) 15.9 ± 1.3 mmHg in intact and 22.3 ± 2.7 mmHg in SAD
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ISSN: | 0193-1849 1522-1555 |
DOI: | 10.1152/ajpendo.2001.280.2.e349 |