title: Atrial natriuretic peptide enhances activity of potassium conductance in adrenal glomerulosa cells.
abstract: Aldosterone secretion from the adrenal glomerulosa (AG) cells is inhibited by atrial natriuretic peptide (ANP). Inasmuch as alterations in K+ conductance can modulate aldosterone secretion, the effect of ANP on intracellular K+ homeostasis was investigated. Intracellular K+ concentration ([K+]i) of AG cells was assessed by spectrofluorometry using the K(+)-sensitive dye, K(+)-binding benzofuran isophthalate. The resting value of [K+]i in AG cells was determined to be 120 +/- 1.2 mM (n = 37) in a HCO3-free, N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid-buffered medium. Exposure of AG cells to ANP led to a dose-dependent, transient decrease in [K+]i, from 21 +/- 3.2% (n = 7) at 100 pM to 31 +/- 2.3% at 1 microM (n = 7). In the continued presence of ANP, a rapid recovery to near basal values of [K+]i was attained within 90 s. Measurements of membrane voltage using the potential sensitive dye 1-3(-sulfonatopropyl)-4-[beta-(-(di-n-butylamino)-6-naphthyl)vinyl ]- pyridinium betaine documented an accompanying change in membrane potential. Pretreatment of AG cells with barium (0.5 mM), tetraethylammonium (0.1 mM), charybdotoxin (100 nM), or ethylene glycol-bis(beta-aminoethylether)-N,N,N',N'-tetraacetic acid (0.5 mM) blunted the ANP-induced decrease in [K+]i. ANP-(7-23), the ANP-C-receptor selective agonist, which does not elevate guanosine 3',5'-cyclic monophosphate (cGMP) did not alter [K+]i in contrast to cGMP (50 microM), which did. We conclude that ANP via the activation of the ANP A receptor alters K+ homeostasis through a Ca(2+)-activatable K(+)-conductive pathway likely to be the maxi-K channel.
authors.affiliation: Department of Medicine, Case Western Reserve University, Cleveland Veterans Affairs Medical Center, Ohio 44106.
authors.forename: M B
authors.initials: MB
authors.lastname: Ganz
authors.forename: J J
authors.initials: JJ
authors.lastname: Nee
authors.forename: C M
authors.initials: CM
authors.lastname: Isales
authors.forename: P Q
authors.initials: PQ
authors.lastname: Barrett
mesh_terms: D000818:Animals; D009320:Atrial Natriuretic Factor / Q000494:pharmacology*; D001464:Barium / Q000494:pharmacology; D002417:Cattle; D002478:Cells, Cultured; D018999:Charybdotoxin; D006152:Cyclic GMP / Q000378:metabolism; D004533:Egtazic Acid / Q000494:pharmacology; D006162:Guanylate Cyclase / Q000378:metabolism; D006706:Homeostasis / Q000187:drug effects; D007700:Kinetics; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D010446:Peptide Fragments / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism*; D026902:Potassium Channel Blockers; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology*; D017461:Receptors, Atrial Natriuretic Factor / Q000378:metabolism; D012604:Scorpion Venoms / Q000494:pharmacology; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000494:pharmacology; D015384:Zona Glomerulosa / Q000187:drug effects / Q000502:physiology*
chemical_list: D010446:Peptide Fragments; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D012604:Scorpion Venoms; D013757:Tetraethylammonium Compounds; D018999:Charybdotoxin; D001464:Barium; D004533:Egtazic Acid; D019789:Tetraethylammonium; D009320:Atrial Natriuretic Factor; C057820:atrial natriuretic factor (7-23); D006162:Guanylate Cyclase; D017461:Receptors, Atrial Natriuretic Factor; D006152:Cyclic GMP; D011188:Potassium