TYPES OF POTASSIUM CHANNELS INVOLVED IN CORONARY REACTIVE HYPEREMIA DEPEND ON DURATION OF PRECEDING ISCHEMIA IN RAT HEARTS

This study was undertaken to clarify factors other than nitric oxide i nvolved in reactive hyperemia after a short(30 sec) and a long(300 sec ) coronary global no-flow ischemia in isolated rat hearts perfused at a constant pressure(90 mmHg) with special focuses on the contribution of various K channels including large and small conductance Ca-activat ed K(KCa) channels as well as ATP-sensitive K(KATP) channels. Reactive hyperemia was induced following 30 sec and 300 sec of no-flow ischemi a of the heart. Coronary reactive hyperemia was observed even after th e inhibition of nitric oxide synthase by N-omega-nitro-L-arginine meth ylester(L-NAME). Selected K channel blockers, none of which affected t he basal flow, were used to evaluate contribution of K channels to thi s L-NAME-resistant reactive hyperemia. After 30-sec ischemia, tetraeth ylammonium(TEA : a non-selective K channel blocker), glibenclamide(Gli : a KATP channel blocker) and a,p-methylene adenosine 5'-diphosphonate (AOPCP: an inhibitor of ecto 5'-nucleotidase) all suppressed both peak flow/basal flow(%PF) and repayment of flow debt(%RFD); After 300-sec ischemia, TEA and charybdotoxin(ChTX: a large conductance KCa channel blocker) decreased %PF and %RFD; AOPCP decreased both %RFD and duratio n, 4-aminopyridine(a voltage-dependent K channel blocker) decreased on ly duration. Neither apamin(a small conductance KCa channel blocker) n or indomethacin(a cyclooxygenase inhibitor) affected the both types of reactive hyperemia. These finding suggest that opening of KATP channe l contributes to coronary vasodilation in reactive hyperemia after sho rt 30-sec ischemia, and that opening of KCa, but not KATP, channel con tributes to it after long 300-sec ischemia. These results also suggest that adenosine may partly be involved in both types of reactive hyper emia.