Effects of adenosine A2 receptor agonists on the excitation of capsaicin-sensitive afferent sensory nerves in airway tissues |
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Authors: | Hiroshi Morimoto Masakatsu Yamashita Katsunori Imazumi Atsushi Matsida Takehiro Ochi Nobuo Seki Hidekazu Mizuhara Takashi Fujii Hachiro Senoh |
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Affiliation: | 1 Department of Pharmacology, New Drug Research Laboratories, Fujisawa Pharmaceutical Co., Ltd., 1-6, 2-chome, Kashima, Yodogawa-ku, Osaka 532, Japan |
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Abstract: | We examined the effects of adenosine analogues on the asthmatic reactions induced by the stimulation of capsaicin-sensitive afferent sensory nerves. Intravenous (i.v.) injection of adenosine A2 receptor agonists, 5′-(N-ethylcarboxamido)-adenosine (NECA) and 2-[p-(carboxyethyl)-phenylethylamino]-5′-N-ethylcarboxamido-adenosine (CGS 21680), dose dependently inhibited capsaicin-induced guinea-pig bronchoconstriction (1–1000 nmol kg−1), whereas i.v. administration of the adenosine A1 receptor agonist, N6-cyclo-hexyladenosine (CHA), did not affect it (1000 nmol kg−1). Intratracheal injection of NECA (0.05–5 nmol site−1) and CGA 21 680 (0.05−5 nmol site−1) also reduced capsaicin-induced constriction in a dose-dependent manner. However, NECA (1000 nmol kg−1) failed to inhibit substance P-induced guinea-pig bronchoconstriction. NECA (1–1000 nmol kg−1) dose-dependently inhibited cigarette smoke-induced rat tracheal plasma extravasation, but not substance P-induced reaction. NECA (0.1–10 μM) and CGS 21 680 (10 μM) significantly blocked the capsaicin-induced release of substance P-like immunoreactivity from guinea-pig lung, whereas CHA (10 μM) had no effect. This evidence suggests that adenosine A2 receptors modulate negatively the excitation of capsaicin-sensitive afferent sensory nerves and substance P release from their endings in airway tissues. |
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