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Department of Pharmacology, University of Virginia School of Medicine, Charlottesville, Virginia 22908
Independently, plasma K+
and ANG II stimulate aldosterone secretion from adrenal glomerulosa
(AG) cells, but together they synergistically control production. We
studied mechanisms to mediate this synergy using bovine AG cells
studied under physiological conditions (in 1.25 mM
Ca2+ at 37°C). Increasing
K+ from 2 to 5 mM caused a
potentiation of ANG II-induced aldosterone secretion and a substantial
membrane depolarization (~21 mV). ANG II inhibited a
K+-selective conductance in both 2 and 5 mM K+ but caused only a
slight depolarization because, under both conditions, membrane
potential was close to the reversal potential of the ANG II-induced
current. ANG II activated calcium/calmodulin-dependent protein kinase
II (CaMKII) equivalently in 2 and 5 mM
K+. However, CaMKII activation
caused a hyperpolarizing shift in the activation of T-type
Ca2+ channels, such that
substantially more current was elicited at membrane potentials
established by 5 mM K+. We propose
that synergy in aldosterone secretion results from K+-induced depolarization and ANG
II-induced modulation of T-type channel activation, such that together
they promote enhanced steady-state Ca2+ flux.
low-voltage-activated calcium channels; calcium/calmodulin-dependent protein kinase II; membrane potential; potassium channels
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