Role of potassium channels in the relaxation induced by the nitric oxide (NO) donor DEA/NO in the isolated rat basilar artery. 
This study investigates whether potassium ion (K+) channels are involved in the nitric oxide (NO)-induced relaxation in segments of the isolated rat basilar artery, mounted onto a wire myograph.  A high extracellular K+ concentration partly inhibited the relaxant effects of the NO donors DEA/NO and SIN-1 (3-morpholino-sydnonimine).  Whereas single applications of the K+ channel inhibitors tetraethyl-ammonium (10(-3) M), glibenclamide (10(-6) M), 4-aminopyridine (10(-3) M), or BaCl(2) (5 x 10(-5) M) did not affect the responses to DEA/NO, a combination of these inhibitors reduced the effects of DEA/NO.  These data suggest, that the relaxant effects of NO donors are partly mediated via activation of K+channels.  Different K+ channel types seem to be involved that function in a redundant manner and compensate for each other.