ISSN:
1432-1912
Keywords:
45Ca2+ Influx
;
Catecholamines
;
22Na+ Influx
;
86Rb+ Uptake
;
Secretion
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Summary In bovine adrenal medullary cells, we reported that 22Na+ influx via nicotinic receptor-associated Na+ channels is involved in 45Ca2+ influx, a requisite for initiating the secretion of catecholamines (Wada et al. 1984, 1985b). In the present study, we investigated whether the inhibition of Na+-pump modulates carbachol-induced 22Na+ influx, 45Ca2+ influx and catecholamine secretion in cultured bovine adrenal medullary cells. We also measured 86Rb+ uptake by the cells to estimate the activity of Na+, K+-ATPase. (1) Ouabain and extracellular K+ deprivation remarkably potentiated carbachol-induced 22Na+ influx, 45Ca2+ influx and catecholamine secretion; this potentiation of carbachol-induced 45Ca2+ influx and catecholamine secretion was not observed in Na+ free medium. (2) Carbachol increased the uptake of 86Rb+; this increase was inhibited by hexamethonium and d-tubocurarine. In Na+ free medium, carbachol failed to increase 86Rb+ uptake. (3) Ouabain inhibited carbachol-induced 86Rb+ uptake in a concentration-dependent manner, as it increased the accumulation of cellular 22Na+. These results suggest that Na+ influx via nicotinic receptor-associated Na+ channels increases the activity of Na+, K+-ATPase and the inhibition of Na+, K+-ATPase augmented carbachol-induced Ca2+ influx and catecholamine secretion by potentiating cellular accumulation of Na+. It seems that nicotinic receptor-associated Na+ channels and Na+, K+-ATPase, both modulate the influx of Ca2+ and secretion of catecholamines by accomodating cellular concentration of Na+.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00500086
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