CALCIUM-ACTIVATED POTASSIUM CHANNEL-MEDIATED ARTERIOLAR RELAXATION DURING ENDOTOXIC-SHOCK

The role of calcium-activated potassium (K-Ca) channels in the in vivo relaxation of arterioles was investigated before endotoxin shock (Pre -ENDT) and during endotoxin shock at 180 min (Post-ENDT). Diameters of 2nd and 3rd order (A(2) and A(3)) arterioles in the left cremaster mu scle of male Sprague-Dawley rats anesthetized with pentobarbital sodiu m were measured using videomicroscopy. Adenosine (ADO) at 534 mu g int raarterially, topical ADO at 10(-3) M, and the endothelium-dependent a gonist topical acetylcholine (AGH) at 10(-4) M significantly dilated b oth A(2) and A(3) arterioles Pre-ENDT and Post-ENDT. Topical tetraethy lammonium chloride (TEA) al 1 mM blocked ADO (intraarterially and topi cal)-induced A(2) and A(3) arteriolar dilations Pre-ENDT and Post-ENDT . Arteriolar dilation to ACH was maintained Pre-ENDT, but was blocked by TEA in A(2) and A(3) arterioles Post-ENDT. The endothelium-independ ent agonist sodium nitroprusside (10(-5) M), when topically applied, c aused maximal arteriolar dilation Pre-ENDT and Post-ENDT in the presen ce of TEA. The data show that vascular smooth muscle K-Ca channels are a significant factor in ADO-induced relaxation of cremaster microvess els and are not significantly affected by ENDT, The results also sugge st that the mechanism for endo thelium-dependent ACH vasodilation chan ges from a non-K-Ca channel-mediated mechanism Pre-ENDT to a K-Ca-medi ated mechanism Post-ENDT.