Influences of Extracellular Calcium and Potassium Concentrations on Adrenaline Release and Membrane Potential in the Perfused Adrenal Medulla of the Rat

Abstract

Prolonged perfusion of isolated rat adrenal glands with high K produced a transient increase in adrenaline 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 was relation obtained: the slope determined in the presence of 5 mM-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 .

Chromaffin cell action potentials and their possible role in adrenaline secretion from rat adrenal medulla.

“…The progressive loss of spike activity at high KCl concentrations may be due to voltage dependent inactivation of the Na channel (Hodgkin & Huxley, 1952). At a KCl concentration of 30 mM the resting membrane potential of the rat adrenal chromaffin cell is approximately -27 mV, compared to -50 mV in control saline Y. KIDOKORO AND A. K. RITCHIE (Ishikawa & Kanno, 1978). The progressive inactivation may also partially contribute to the decline in peak spike amplitude as the KCl concentration is raised (e.g.…”

“…The actions of KCl on spike frequency are probably a consequence of the ability of KCl to depolarize the chromaffin cell membrane (Ishikawa & Kanno, 1978;. Low concentrations of ACh also increase spike frequency but do not seem to depolarize the chromaffin cell membrane in a similar manner to KCl (Brandt et al 1976).…”

“…Secretion can also be evoked by external perfusion with ACh (Douglas & Rubin, 1961) or depolarizing concentrations of KCl (Douglas & Rubin, 1961;Ishikawa & Kanno, 1978;Kidokoro, Ritchie & Hagiwara, 1979). In each instance release requires external Ca ions (Douglas & Rubin, 1961;Ishikawa & Kanno, 1978).…”

“…Secretion can also be evoked by external perfusion with ACh (Douglas & Rubin, 1961) or depolarizing concentrations of KCl (Douglas & Rubin, 1961;Ishikawa & Kanno, 1978;Kidokoro, Ritchie & Hagiwara, 1979). In each instance release requires external Ca ions (Douglas & Rubin, 1961;Ishikawa & Kanno, 1978). During long term depolarization (several minutes) the entry of Ca into the cell Stallcup, 1979) and subsequent secretion Ritchie, 1979) is apparently mediated by influx through slowly inactivating voltage dependent Ca channels.…”

Sodium‐dependent inhibition by PN200‐110 enantiomers of nicotinic adrenal catecholamine release

“…While some authors conclude that the influx of Ca through voltage dependent channels is the common ionic event in triggering catecholamine release evoked either by K, veratridine or nicotinic receptor stimulation (Cefia et al, 1983;Wada et al, 1985), others suggest a major contribution of receptor-operated channels (Douglas & Rubin, 1963;Ishikawa & Kanno, 1978;Holz et al, 1982;Kilpatrick et al, 1982).…”