Tetraethylammonium-evoked oscillatory contractions of rat tail artery: A K-K model

Spontaneously rhythmic contraction of peripheral blood vessels actively mod ulates the peripheral circulation and blood pressure. However, the underlyi ng mechanisms for the complex rhythmic contraction patterns of various vasc ular tissues are not yet fully understood. In the present study, the tetrae thylammonium (TEA)-induced spontaneously oscillatory contractions of isolat ed rat tail artery tissues were examined. It was found that TEA evoked arte rial oscillatory contractions in a concentration-dependent, but endothelium -independent manner. The voltage- dependent K+ (Kv) channel specific blocke r, 4-aminopyridine (4-AP), induced a sustained, but not oscillated, vascula r contraction. The presence of 4-AP had no effect on the TEA-induced oscill atory contractions. The blockade of K-Ca channels with charybdotoxin or apa min did not affect the basal force of vascular tissues. Neither the TEA-ind uced oscillatory contraction was affected by these blockers. The opening of K-ATP channels by levcromakalim or their blockade by glybenclamide ceased or increased, respectively, the oscillation of TEA-induced contractions. Th e absence of Ca2+ or the presence of nifedipine in the bath solution comple tely abolished the effects of TEA. The inhibition of Ca2+-ATPase in the sar coplasmic reticulum with micromolar concentrations of thapsigargin or cyclo piazonic acid either abolished or enhanced, respectively, the TEA-induced o scillatory contractions. Ryanodine did not affect the TEA-induced oscillato ry contraction. In conclusion, the TEA-induced oscillatory contraction may be initiated by the blockade of the TEA-sensitive delayed rectifier K+ chan nels and maintained by the TEA-insensitive but ATP-sensitive K+ channels. T his K-K model presents a novel mechanism for the depolarization-induced rhy thmic contractions of small arteries.