Nitric Oxide Inhibits the Bradykinin B2 Receptor-Mediated Adrenomedullary Catecholamine Release but Has No Effect Adrenal Blood Flow Response In Vivo

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  • Bouallegue Ali
    The Autonomic Nervous System Research Group, Faculty of Pharmacy, University of Montreal
  • Yamaguchi Nobuharu
    The Autonomic Nervous System Research Group, Faculty of Pharmacy, University of Montreal

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  • Nitric Oxide Inhibits the Bradykinin B2 Receptor-Mediated Adrenomedullary Catecholamine Release but Has No Effect on Adrenal Blood Flow Response In Vivo

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The role of nitric oxide (NO) in bradykinin (BK)-induced adrenal catecholamine secretion still remains obscure. The present study was to investigate whether an inhibition of NO synthase with Nω-nitro-<sc>L</sc>-arginine methyl ester (<sc>L</sc>-NAME) would modulate BK-induced adrenal catecholamine secretion (ACS) and adrenal vasodilating response (AVR) in anesthetized dogs. Plasma catecholamine concentrations were determined with an HPLC coupled with an electrochemical detector. All drugs were locally administered to the left adrenal gland via intra-arterial infusion. BK dose-dependently increased both ACS and AVR. Hoe-140, a selective B2 antagonist, significantly blocked the BK-induced increases in both ACS and AVR. In the presence of <sc>L</sc>-NAME, the BK-induced ACS was significantly enhanced, while the simultaneous AVR remained unaffected. These results suggest that the both BK-induced ACS and AVR are primarily mediated by B2 receptors in the canine adrenal gland. Our results also suggest that the enhanced ACS in response to BK in the presence of <sc>L</sc>-NAME may have resulted from a specific inhibition of NO formation in the adrenal gland. It is concluded that the BK-induced NO may play an inhibitory role in the B2-receptor-mediated mechanisms regulating ACS, while it may not be implicated in the B2-receptor-mediated AVR under in vivo conditions.<br>

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