Bradykinin (BK, 0.03-1 μg), capsaicin (1 μg) or potassium chloride (KCl, 13 μmol) applied to the epicardium of the left ventricle of anaesthetized, open-chest dogs, caused reflex tachycardia and pressor effects, whereas des-Arg9-Bk (1-100 μg), a selective bradykinin B1-receptor agonist, failed to produce any cardiovascular response. Superfusion of the epicardium with a selective B1-receptor antagonist, des-Arg9-[Leu8]BK (50-100 μg/min) had no effect on reflex responses to epicardial BK (0.03-0.1 μg). However, the selective B2-receptor antagonist, D-Arg-[Hyp3, Thi5,8, D-Phe7] BK (10-25 μg/min) abolished the reflex effects of 0.03 and 0.1 μg BK and reduced by 50 to 70% the responses to 1 μg BK. Another B2-receptor antagonist [Thi6,9, D-Phe8]kallidin (10-50 μg/min) alson reduced (30-70%) responses to 1 μg BK. The antagonism was reversible and specific for BK since reflex responses to epicardial application of either capsaicin or KCl were not affected. The results indicate that BK interacts with B2-receptors, probably located on terminals and/or axons of sympathetic afferents supplying the dog heart, to activate a cardiac sympathetic chemoreflex. © 1988.
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