REGULATION OF ADRENERGIC NERVE-MEDIATED CONTRACTION OF CANINE PULMONARY-ARTERY BY K+ CHANNELS

The aim of the present study was to investigate the role of certain su btypes of K+ channels in nerve-evoked contractions of pulmonary artery ill vitro. The lobar or segmental pulmonary arteries were dissected f rom dogs, cut into ring segments, and the contractile responses to ele ctrical held stimulation (EFS) and noradrenaline were measured under i sometric conditions. Addition of iberiotoxin, a big conductance Ca2+-a ctivated K channel blocker, and apamin, a small conductance Ca2+-activ ated K+ channel blocker, did not change the resting tension but augmen ted the contractile responses to EFS, so that the electric stimulus fr equency required to produce a half-maximal contraction (ES50) was decr eased from 18.2 +/- 3.5 to 7.4 +/- 2.3 Hz (p < 0.01) and from 16.8 +/- 2.2 to 11.4 +/- 2.0 Hz (p , 0.05), respectively, whereas glibenclamid e, an adenosine triphosphate (ATP)-sensitive K+ channel blocker, had n o effect. In contrast, none of the K+ channel blockers altered the con tractile response to noradrenaline. Incubation of tissues with iberiot oxin and apamin increased the release of H-3-noradrenaline evoked by E FS. We conclude that big conductance Ca2+-activated K+ channels and sm all conductance Ca2+-activated K+ channels may play a role in the regu lation of adrenergic neurotransmission in the pulmonary artery, probab ly by inhibiting the exocytotic release of noradrenaline from the adre nergic nerve terminals.