SUBARACHNOID HEMORRHAGE AND THE ROLE OF POTASSIUM CHANNELS IN RELAXATIONS OF CANINE BASILAR ARTERY TO NITROVASODILATORS

This study was designed iu determine the effect of subarachnoid hemorr hage (SAH) on potassium (K+) channels involved in relaxations of cereb ral arteries to nitrovasodilators. The effects of K+ channel inhibitor s on relaxations to 3-morpholinosydnonimine (SIN-1) and sodium nitropr usside (SNP) were studied in rings of basilar arteries obtained from u ntreated dogs and dogs exposed to SAH. The levels of cyclic GMP were m easured by radioimmunoassay. In rings without endothelium, concentrati on-dependent relaxations to SIN-1 (10(-9) - 10(-4) mol/L) and SNP (10( -9) - 10(-4) mol/L) were not affected by SAH, whereas increase in cycl ic GMP production stimulated by SIN-1 (10(-6) mol/L) was significantly suppressed after SAH. The relaxations to SIN-1 and SNP were reduced b y charybdotoxin (CTX: 10(-7) mol/L), a selective Ca2+-activated K+ cha nnel inhibitor, in both normal and SAH arteries: however, the reductio n of relaxations by CTX was significantly greater in SAH arteries, By contrast, the relaxations to these nitrovasodilators were not affected by glyburide (10(-5) mol/L), an ATP-sensitive K+ channel inhibitor, i n both normal and SAH arteries. These findings suggest that in cerebra l arteries exposed to SAH, Ca2+-activated K+ channels may play a compe nsatory role in mediation of relaxations to nitric oxide. This may hel p to explain mechanisms of relaxations to nitrovasodilators in arterie s with impaired production of cyclic GMP.