Abstract
The effects of noradrenaline and of raised external potassium ([K+]o) on the efflux of 86Rb or 42K and on tension were studied in preparations taken from eight different arteries under various conditions. There was a 10-fold variation in the maximum 86Rb efflux evoked by noradrenaline (10(-5)-10(-4) M) in the arteries studied, even though tension generated was comparable. Arterial contractions were either accompanied by large increases in 86Rb efflux, e.g. rabbit ear artery and aorta, guinea-pig and rabbit pulmonary artery, or by small increases, e.g. rabbit and guinea-pig mesenteric artery, rabbit brachial artery and guinea-pig abdominal aorta. Raising [K+]o also had a diverse effect on 86Rb and 42K efflux: arteries giving small increases in efflux to noradrenaline also gave small increases in efflux to raised [K+]o. The maximum efflux evoked by raised [K+]o was on average three times greater than the maximum efflux evoked by noradrenaline in the arteries studied. The heterogeneity of the efflux response could not be explained by the quantitative heterogeneity of the efflux response could not be explained by the quantitative differences in the effects of noradrenaline or of raised [K+]o on membrane potential or, in the case of noradrenaline, by differences in the alpha-receptors. In arteries in which the noradrenaline-evoked 86Rb efflux was small, histamine, 5-hydroxytryptamine, vasopressin and angiotensin also had little effect. Conversely, where noradrenaline produced a large increase in 86Rb efflux those other stimulants had comparable effects. Removal of extracellular calcium only slightly reduced the increment in 86Rb efflux evoked by 66 mM-external K+ in the rabbit aorta even though contractions were virtually abolished under these conditions. In the case of 10(-5) M-noradrenaline, 40% of the contraction remained and its effect on efflux was significantly increased (P less than 0.05) in calcium-free conditions. Essentially similar results were obtained using 42K. Tetraethylammonium (10-20 mM) produced a significant and substantial reduction (P less than 0.001) in the 86Rb efflux evoked by raised [K+]o while only slightly affecting the noradrenaline-evoked efflux in the rabbit aorta. It was concluded from these efflux experiments on vascular muscle that the channels through which potassium can escape, opened by depolarization and by activation of alpha-receptors with noradrenaline, are from different populations, and that their properties vary from one artery to another. We have been unable to detect any substantial calcium-activated component in 42K or 86Rb efflux responses to raised [K+]o or to noradrenaline.