Characterization of angiotensin II-regulated K+ conductance in rat adrenal glomerulosa cells.
Nystatin perforated-patch clamp and single-channel recording methods were used to characterize macroscopic and single-channel K+ currents and the effects of angiotensin II (AngII) in cultured rat adrenal glomerulosa cells. Two basic patterns of macroscopic current-voltage relationships were observed: type 1 exhibited a rapidly activating, noninactivating, voltage-dependent outward current and type 2 exhibited an inactivating voltage-dependent outward current attributed to charybdotoxin sensitive Ca++-dependent K+ channels. Most cells exhibited the type 1 pattern and experiments focused on this cell type. Cell-attached and inside-out patches were dominated by a single K+ channel class which exhibited an outward conductance of 12 pS (20 mm K+ pipette in cell-attached and inside-out configurations, 145 mm K+in), a mean open time of 2 msec, and a weakly voltage-dependent low open probability that increased with depolarization. Channel open probability was reversibly inhibited by bath stimulation with AngII. At the macroscopic level, type 1 cell macroscopic K+ currents appeared comprised of two components: a weakly voltage-dependent current controlling the resting membrane potential (-85 mV) which appeared mediated by the 12 pS K+ channel and a rapidly activating, noninactivating voltage-dependent current activated above -50 mV. The presence of the second voltage-dependent K+ channel class was suggested by the effects of AngII, the blocking effects of quinidine and Cs+, and the properties of the weakly voltage-dependent K+ channel described. The K+ selectivity of the macroscopic current was demonstrated by the dependence of current reversal potentials on the K+ equilibrium potential and by the effects of K+ channel blockers, Cs+ and quinidine. AngII (10 pm to 1 nm) reversibly inhibited macroscopic K+ currents and this effect was blocked by the AT1 receptor antagonist losartin.
Lotshaw
D P
DP
Department of Biological Sciences, Northern Illinois University, DeKalb, IL 60115, USA.
D000450:Aldosterone / Q000378:metabolism; D000804:Angiotensin II / Q000502:physiology*; D000818:Animals; D001713:Biphenyl Compounds / Q000494:pharmacology; D002478:Cells, Cultured; D002586:Cesium / Q000494:pharmacology; D005260:Female; D007093:Imidazoles / Q000494:pharmacology; D017136:Ion Transport; D019808:Losartan; D008564:Membrane Potentials / Q000187:drug effects; D009761:Nystatin / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D011188:Potassium / Q000378:metabolism; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology*; D011802:Quinidine / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction / Q000187:drug effects; D013777:Tetrazoles / Q000494:pharmacology; D015384:Zona Glomerulosa / Q000166:cytology / Q000378:metabolism*
D001713:Biphenyl Compounds; D007093:Imidazoles; D015221:Potassium Channels; D013777:Tetrazoles; C087375:charybdotoxin receptor; D000804:Angiotensin II; D009761:Nystatin; D002586:Cesium; D000450:Aldosterone; D011802:Quinidine; D019808:Losartan; D011188:Potassium