Characterization of K+ and Ca2+ ionic currents in glomerulosa cells from human adrenal glands.
Ionic currents of primary cultured glomerulosa cells from human adrenal glands were studied with the patch-clamp technique. Two types of outward K+ currents and two types of inward Ca2+ currents were described. The transient outward K+ current activated at potential positive to -40 mV and demonstrated a marked time-dependent inactivation. It was blocked by 4-aminopyridine but not tetraethylammonium. A second type of outward current activated rapidly at the depolarization onset and then increased slowly with no time-dependent inactivation. The transient inward T-type Ca2+ current was activated for potential positive to -60 mV with a maximal current amplitude at -30 mV and zero current voltage at +40 mV; it was completely inactivated for membrane potential positive to -40 mV. The pharmacological studies of the T-type channel showed that Ni2+ was a potent blocker but that the channel was not sensitive to dihydropyridine. The long-lasting inward Ca2+ current was activated for potentials positive to -20 mV with a maximum current amplitude at +70 mV. This current was increased by the agonist Bay K 8644 and blocked by the antagonist nifedipine; in addition, it was blocked by Cd2+ but less sensitive to Ni2+. This study revealed that glomerulosa cells from human adrenal demonstrated the presence of K+ and Ca2+ currents similar to those found in rat and bovine cells. Moreover, the main stimuli of aldosterone secretion, ACTH and angiotensin II, induce an increase in aldosterone secretion which is inhibited in a Ca(2+)-free external medium.
Payet
M D
MD
Département de Physiologie et Biophysique, Faculté de Médecine, Université de Sherbrooke, Quebec, Canada.
Durroux
T
T
Bilodeau
L
L
Guillon
G
G
Gallo-Payet
N
N
D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / Q000494:pharmacology; D015761:4-Aminopyridine / Q000494:pharmacology; D000200:Action Potentials; D000293:Adolescent; D000328:Adult; D000450:Aldosterone / Q000378:metabolism; D001464:Barium / Q000378:metabolism; D002104:Cadmium / Q000494:pharmacology; D015220:Calcium Channels / Q000187:drug effects / Q000502:physiology*; D002478:Cells, Cultured; D004553:Electric Conductivity; D006801:Humans; D007700:Kinetics; D008564:Membrane Potentials; D009532:Nickel / Q000494:pharmacology; D009543:Nifedipine / Q000494:pharmacology; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology*; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000494:pharmacology; D015384:Zona Glomerulosa / Q000187:drug effects / Q000502:physiology*
D015220:Calcium Channels; D015221:Potassium Channels; D013757:Tetraethylammonium Compounds; D002104:Cadmium; D001464:Barium; D000450:Aldosterone; D019789:Tetraethylammonium; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D009532:Nickel; D015761:4-Aminopyridine; D009543:Nifedipine