Abstract
Prolonged perfusion of isolated rat adrenal glands with high K produced a transient increase in adrenaline [epinephrine] release that reached a maximum within 1 min and then declined with a half-time of about 5 min. The higher the [K]o used, the larger was the release of adrenaline elicited. There was a linear relation between the mean rate of adrenaline release in the initial 5 min of continuous stimulation with excess K and logarithmic increase in the [K]o. The higher the [Ca]o used, the steeper the relation obtained: the slope determined in the presence of 5mM-Ca was nearly twice as much as that obtained in the presence of 0.5 mM-Ca. The release of adrenaline in response to excess K was virtually abolished by the omission of [Ca]o. The chromaffin cells were depolarized in proportion to logarithmic increase in the [K]o. Linear relations were thus obtained between the mean rates of adrenaline release and the membrane potential of chromaffin cells in the presence of different [Ca]o. Application of high K revived secretory response of a gland after prolonged exposure to acetylcholine in the presence of tetrodotoxin, when adrenaline release had declined below a half of the maximum response. Application of acetylcholine also revived secretory response after prolonged exposure to high K. The mechanism of Ca influx activated by high K may differ from that activated by acetylcholine.