Atrial natriuretic peptide enhances activity of potassium conductance in adrenal glomerulosa cells

M. B. Ganz, J. J. Nee, C. M. Isales, P. Q. Barrett

Research output: Contribution to journalArticle

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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 μM (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-{β-(-(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(β-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 μM), which did. We conclude that ANP via the activation of the ANP A receptor alters K+ homeostasis through a Ca2+-activatable K+-conductive pathway likely to be the maxi-K channel.

Original languageEnglish (US)
Pages (from-to)1357-1365
Number of pages9
JournalAM.J.PHYSIOL.
Volume266
Issue number5 part 1
StatePublished - May 13 1994

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Zona Glomerulosa
Atrial Natriuretic Factor
Potassium
Atrial Natriuretic Factor Receptors
Aldosterone
Homeostasis
Coloring Agents
Charybdotoxin
Large-Conductance Calcium-Activated Potassium Channels
HEPES
Betaine
Tetraethylammonium
Ethylene Glycol
Fluorescence Spectrometry
Cyclic GMP
Barium
Membranes
Membrane Potentials
Acids
Chemical activation

Keywords

  • intracellular potassium
  • membrane potential
  • potassium-binding benzofuran isophthalate

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Cell Biology
  • Physiology

Cite this

Atrial natriuretic peptide enhances activity of potassium conductance in adrenal glomerulosa cells. / Ganz, M. B.; Nee, J. J.; Isales, C. M.; Barrett, P. Q.

In: AM.J.PHYSIOL., Vol. 266, No. 5 part 1, 13.05.1994, p. 1357-1365.

Research output: Contribution to journalArticle

Ganz, MB, Nee, JJ, Isales, CM & Barrett, PQ 1994, 'Atrial natriuretic peptide enhances activity of potassium conductance in adrenal glomerulosa cells', AM.J.PHYSIOL., vol. 266, no. 5 part 1, pp. 1357-1365.
Ganz, M. B. ; Nee, J. J. ; Isales, C. M. ; Barrett, P. Q. / Atrial natriuretic peptide enhances activity of potassium conductance in adrenal glomerulosa cells. In: AM.J.PHYSIOL. 1994 ; Vol. 266, No. 5 part 1. pp. 1357-1365.
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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 μM (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-{β-(-(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(β-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 μM), which did. We conclude that ANP via the activation of the ANP A receptor alters K+ homeostasis through a Ca2+-activatable K+-conductive pathway likely to be the maxi-K channel.",
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N2 - 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 μM (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-{β-(-(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(β-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 μM), which did. We conclude that ANP via the activation of the ANP A receptor alters K+ homeostasis through a Ca2+-activatable K+-conductive pathway likely to be the maxi-K channel.

AB - 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 μM (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-{β-(-(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(β-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 μM), which did. We conclude that ANP via the activation of the ANP A receptor alters K+ homeostasis through a Ca2+-activatable K+-conductive pathway likely to be the maxi-K channel.

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