Potassium-induced endothelium-dependent rhythmic activity in the canine basilar artery

Abstract

Rings of canine basilar arteries with and without endothelium were suspended for isometric tension recording in modified Krebs-Ringer bicarbonate solution. Increased extracellular concentrations of potassium (3-20 mM) caused rhythmic activity in rings with endothelium. This activity was reduced by the removal of the endothelium and by exposure to indomethacin, meclofenamate, diltiazem, or ouabain; it was not affected by tetrodotoxin, bretylium tosylate, phentolamine, propranolol, atropine, methiothepin, and cimetidine. Prostaglandin F(2α) and E2 caused concentration-dependent increases in the frequency and the amplitude of this rhythmic activity and reversed the inhibitory effect of indomethacin and meclofenamate. Prostacyclin abolished the activity. These results suggest that increasing the concentration of extracellular potassium causes rhythmic activity in canine basilar arteries because of the production and/or release by the endothelium of products of cyclooxygenase such as prostaglandin F(2α) and E2. These may initiate the contraction while prostacyclin triggers the relaxation phase of rhythmic activity, possibly by activating Na+, K+-ATPase of the vascular smooth muscle.