Correlation Between Catecholamine Release and Sodium Pump Inhibition in the Perfused Adrenal Gland of the Cat

Abstract

(10-4 M) inhibited the uptake of 86Rb into adreno-medullary tissue by 60%. Maximal inhibition had already occurred 2 min after adding the drug, indicating a lack of temporal correlation between ATPase inhibition and the ouabain secretory response, which took longer (about 30-40 min) to reach its peak. NEM (10-4 M) blocked 86Rb uptake in a similar manner. 6 The results are further evidence in favour of the presence of a Na+-Ca2+ exchange system in the chromaffin cell membrane, probably involved in the control of [Ca2+]i and in the modulation of catecholamine secretion. This system is activated by increasing [Na+]j, either directly (ionophore X537A, increased [Na+]J) or indirectly (Na+ pump inhibition). However, the simple inhibition of Na+ pumping does not always lead to a catecholamine secretory response; such is the case for NEM.

Effects of Bay K 8644 on cat adrenal catecholamine secretory responses to A23187 or ouabain

“…If Bay K 8644 were acting intracellularly in a step beyond the Ca channel, then secretory responses such as those induced by A23187 or activation ofthe Na/Ca exchange mechanism by Kfree solution, ought also to be potentiated by the dihydropyridine. Like ouabain, K deprivation inhibits the membrane Na+,K+-ATPase activity (Skou, 1957) causing the secondary activation by intracellularly accumulated Na, of a membrane Na/Ca exchange carrier that leads to an increased rate of catecholamine release (Garcia et al, 1981b). The experiment demonstrating that Bay K 8644 was unable to affect the profile of the secretory curve obtained with K-free solutions, strongly suggests that this drug is not acting on the Na/Ca exchange system of the chromaffin cell membrane to modify its activity.…”

A small increment of external K concentration accelerates adrenomedullary catecholamine secretion induced by ouabain and metabolic inhibitors.

“…The rate of 45Ca efflux from the medullary slices (RINK, 1977) and the perfused cortex-free medulla (AGUIRRE et a!., 1977) was largely dependent on external Na. Conversely, all the procedures leading to a rise in the concentration of internal Na was found to increase Ca influx in exchange for internal Na (that is, Na-dependent Ca influx) thereby increasing catecholamine (CA) secretion (ESQUERRO et al, 1980;GARCIA et al, 1980GARCIA et al, , 1981bNISHIMURA et al, 1981;SORIMACHI et al, 1981;SORIMACHI and YAMAGAMI, 1983). Recently, GARCIA et al (1981a) reported that ouabain treatment of the adrenal gland enabled a small increment of external K to increase markedly the rate of CA secretion.…”

Cytosolic organelles shape calcium signals and exo–endocytotic responses of chromaffin cells

“…In bovine chromaffin cells NCX1 can favour Na + -dependent Ca 2+ influx [143] or Ca 2+ export [144] and has been proposed to participate in the regulation of [Ca 2+ ] c and exocytosis in cat [150,161,162] and bovine chromaffin cells [142,143,153,[163][164][165]. In addition, chromaffin cells co-express NCX and the retinal rod-type K + -dependent Na + /Ca 2+ exchanger [166].…”