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Thromboxane A2is involved in the nitric oxide-induced central activation of adrenomedullary outflow in rats

Authors
Journal
Neuroscience
0306-4522
Publisher
Elsevier
Publication Date
Volume
87
Issue
1
Identifiers
DOI: 10.1016/s0306-4522(98)00133-x
Keywords
  • Nitric Oxide
  • Thromboxane A2
  • Brain
  • Plasma Adrenaline
  • Plasma Noradrenaline
  • Adrenomedullary Outflow

Abstract

Abstract The central effect of 3-morpholinosydnonimine, a nitric oxide donor, on the sympatho-adrenomedullary system was investigated in urethane-anesthetized rats. Intracerebroventricular administration of 3-morpholinosydnonimine (100, 250 and 500 μg/animal) induced a marked elevation of adrenaline levels and a slight elevation of noradrenaline levels in the plasma. These 3-morpholinosydnonimine (250 μg/animal)-induced elevations of catecholamines were abolished by intracerebroventricular treatments with 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl 3-oxide (750 μg/animal), a nitric oxide scavenger, and indomethacin (500 μg/animal), a cyclo-oxygenase inhibitor, but not with superoxide dismutase (250 units/animal), a superoxide anion scavenger. Furthermore, the 3-morpholinosydnonimine (250 μg/animal)-induced elevation of plasma adrenaline levels was abolished by intracerebroventricular treatments with thromboxane A 2 synthase inhibitors [furegrelate (100, 250 and 1000 μg/animal) and carboxyheptyl imidazole (500 μg/animal)], and also with thromboxane A 2 receptor blockers [(+)-S-145 (100, 250 and 1000 μg/animal) and SQ29548 (8 μg/animal)]. The elevation of noradrenaline levels was, however, not attenuated by these thromboxane A 2-related test agents. The present results indicate that nitric oxide but not peroxynitrite markedly activates central adrenomedullary outflow. Thromboxane A 2 in the brain is probably involved in this central activation of adrenomedullary outflow.

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