Responses of the rat tail artery to high external potassium concentration

The isolated rat artery, exposed to non cumulatively increased potassium concentrations, underwent concentration-related sustained contractions. When potassium was cumulatively elevated, the amplitude of the contractions was significantly lower. Cocaine potentiated the effects of the non cumulatively increased potassium, whereas after alpha-blockade or using reserpine pretreated arteries, the responses were small, short lasting contractions. Reduction of the external sodium to 25 mM, potentiated the responses to the lower range of potassium concentrations and decreased those to the higher concentrations. In alpha-blocked arteries, low-sodium reduced the responses to all the potassium concentrations. The increase of the calcium concentration to 2.5 mM, enhanced the responses to potassium and produced a significant leftward shift of the frequency-response curve to electrical stimulation. These findings indicate that to establish the actual responses to high external potassium, non cumulative dose-response curves must be performed. The actions of potassium are mainly exerted through the release of endogenous catecholamines, the electromechanical coupling seeming to be unable to evoke sustained contractures. The changes of the ionic environment differentially alter the direct and indirect effects of potassium and the release of norepinephrine induced by potassium or by field-electric stimulation, appear to have different ionic requirements.