Open AccessNongenomic Effect of Aldosterone on Ion Transport Pathways of Red Blood Cells
Author(s) -
Lyubomira Ivanova,
Rita Bernhardt,
Ingolf Bernhardt
Publication year - 2008
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000149805
Subject(s) - aldosterone , symporter , chemistry , sodium–hydrogen antiporter , ion transporter , intracellular , transporter , biophysics , medicine , endocrinology , mineralocorticoid , sodium , biochemistry , biology , membrane , organic chemistry , gene
The direct influence of aldosterone on the human and avian red blood cell (RBC) transport systems, Na(+)/K(+) pump, Na(+),K(+),2Cl(-) symporter, and K(+) (Na(+))/H(+) exchanger, was investigated with tracer kinetics. The present work proved that aldosterone has no significant effect on these transport pathways. However, in young human RBCs containing reticulocytes aldosterone showed a significant inhibition of the Na(+),K(+),2Cl(-) symporter. Investigations of the Li(+) efflux via the Na(+)/Li(+) exchanger using atom absorption spectroscopy revealed that aldosterone has no effect on this transporter. Studies of the effect of aldosterone on the Ca(2+) content and the intracellular pH (pH(i)) were carried out on single RBCs with a fluorescence imaging system. Both parameters are affected by aldosterone. The Ca(2+) uptake in the presence of aldosterone, under conditions where the Ca(2+) pump is inhibited, showed marked differences from the control. Since the effect is nifedipine-sensitive, it seems that aldosterone affects a Ca(2+) channel. In addition, aldosterone leads to an acidification of the intracellular medium after an initial alkalisation due to an effect on the Na(+)/H(+) exchanger.