THE ROLE OF THE ENDOCARDIUM IN THE FACILITATORY EFFECT OF BRADYKININ ON ELECTRICALLY-INDUCED RELEASE OF NORADRENALINE IN RAT CARDIAC VENTRICLE

1 The present investigation was undertaken to study the role of bradyk inin in noradrenaline release from the ventricle of the rat induced by electrical stimulation. Slices of the left ventricle of adult Wistar rats with or without endocardium were previously loaded with 0.2 mu M [H-3]-noradrenaline and washed out before electrical stimulation was a pplied. 2 Bradykinin (0.1-100 nM) concentration-dependently increased tritium release evoked by electrical stimulation (EC(50) = 3.5 (1.2-10 .2) nM; n = 12). The angiotensin converting enzyme inhibitor, captopri l (1 mu M), which pet se had no effect on tritium release, caused a ma rked enhancement of the bradykinin facilitatory effect, shifting the c oncentration-response curve of bradykinin to the left by about one log unit. The compound Hoe 140, a selective inhibitor of B-2-bradykinin r eceptors, competitively antagonized the effect of bradykinin, indicati ng the involvement of these receptors in the action of bradykinin. 3 I n endocardium-free ventricle, bradykinin had no effect either in the a bsence or in the presence of captopril. 4 These results show that: (1) bradykinin is able to facilitate noradrenaline release evoked by elec trical stimulation of the rat ventricle through activation of B-2-brad ykinin receptors located on endocardial cells; (2) this action of brad ykinin which is markedly potentiated by the inhibition of the angioten sin-converting enzyme seems to be exerted through the release of some factor which is formed in the endocardium and diffuses into the myocar dium where it acts.