Na+-H+ and Na+-Ca2+ exchange in glomerulosa cells: Possible role in control of aldosterone production

L. Hunyady, S. Kayser, E. J. Cragoe, I. Balla, T. Balla, A. Spät

Research output: Article

20 Citations (Scopus)

Abstract

Sodium uptake by rat adrenal glomerulosa cells was stimulated by intracellular acidosis evoked by Na2+-propionate. This process was inhibited by 5-(N,N-hexamethylene)amiloride (HMA), a known inhibitor of the Na+-H+ exchange. These experiments demonstrate the existence of the Na+-H+ exchange in glomerulosa cells. Although amiloride inhibited the angiotensin II- and adrenocorticotropic hormone (ACTH)-induced aldosterone response, HMA, a more specific inhibitor of Na+-H+ exchange, failed to do that. 45Ca2+ influx and efflux were dependent on intra- and extracellular Na+ concentrations. Amiloride analogues, known to inhibit Na+-Ca2+ exchange, reduced basal 45Ca influx. Although we could not reveal the activation of Na+-Ca2+ exchange by angiotensin II, inhibitors of Na-Ca2+ exchange also inhibited the angiotensin- and ACTH-induced aldosterone response of glomerulosa cells. Our results suggest that Na+-Ca2+ exchange supports the maintenance of basal Ca2+ level in the cytoplasma of glomerulosa cells, and amiloride derivatives inhibit aldosterone production by reducing Ca2+ level below resting values.

Original languageEnglish
JournalAmerican Journal of Physiology - Cell Physiology
Volume254
Issue number6
Publication statusPublished - 1988

Fingerprint

Amiloride
Aldosterone
Angiotensin II
Adrenocorticotropic Hormone
Propionates
Angiotensins
Zona Glomerulosa
Rats
Ion exchange
Acidosis
Sodium
Chemical activation
Derivatives
Maintenance
Experiments
5-(N,N-hexamethylene)amiloride

ASJC Scopus subject areas

  • Cell Biology
  • Clinical Biochemistry
  • Physiology

Cite this

@article{5565262ff25b4678947ca7a16ecaf52f,
title = "Na+-H+ and Na+-Ca2+ exchange in glomerulosa cells: Possible role in control of aldosterone production",
abstract = "Sodium uptake by rat adrenal glomerulosa cells was stimulated by intracellular acidosis evoked by Na2+-propionate. This process was inhibited by 5-(N,N-hexamethylene)amiloride (HMA), a known inhibitor of the Na+-H+ exchange. These experiments demonstrate the existence of the Na+-H+ exchange in glomerulosa cells. Although amiloride inhibited the angiotensin II- and adrenocorticotropic hormone (ACTH)-induced aldosterone response, HMA, a more specific inhibitor of Na+-H+ exchange, failed to do that. 45Ca2+ influx and efflux were dependent on intra- and extracellular Na+ concentrations. Amiloride analogues, known to inhibit Na+-Ca2+ exchange, reduced basal 45Ca influx. Although we could not reveal the activation of Na+-Ca2+ exchange by angiotensin II, inhibitors of Na-Ca2+ exchange also inhibited the angiotensin- and ACTH-induced aldosterone response of glomerulosa cells. Our results suggest that Na+-Ca2+ exchange supports the maintenance of basal Ca2+ level in the cytoplasma of glomerulosa cells, and amiloride derivatives inhibit aldosterone production by reducing Ca2+ level below resting values.",
author = "L. Hunyady and S. Kayser and Cragoe, {E. J.} and I. Balla and T. Balla and A. Sp{\"a}t",
year = "1988",
language = "English",
volume = "254",
journal = "American Journal of Physiology",
issn = "0363-6119",
publisher = "American Physiological Society",
number = "6",

}

TY - JOUR

T1 - Na+-H+ and Na+-Ca2+ exchange in glomerulosa cells

T2 - Possible role in control of aldosterone production

AU - Hunyady, L.

AU - Kayser, S.

AU - Cragoe, E. J.

AU - Balla, I.

AU - Balla, T.

AU - Spät, A.

PY - 1988

Y1 - 1988

N2 - Sodium uptake by rat adrenal glomerulosa cells was stimulated by intracellular acidosis evoked by Na2+-propionate. This process was inhibited by 5-(N,N-hexamethylene)amiloride (HMA), a known inhibitor of the Na+-H+ exchange. These experiments demonstrate the existence of the Na+-H+ exchange in glomerulosa cells. Although amiloride inhibited the angiotensin II- and adrenocorticotropic hormone (ACTH)-induced aldosterone response, HMA, a more specific inhibitor of Na+-H+ exchange, failed to do that. 45Ca2+ influx and efflux were dependent on intra- and extracellular Na+ concentrations. Amiloride analogues, known to inhibit Na+-Ca2+ exchange, reduced basal 45Ca influx. Although we could not reveal the activation of Na+-Ca2+ exchange by angiotensin II, inhibitors of Na-Ca2+ exchange also inhibited the angiotensin- and ACTH-induced aldosterone response of glomerulosa cells. Our results suggest that Na+-Ca2+ exchange supports the maintenance of basal Ca2+ level in the cytoplasma of glomerulosa cells, and amiloride derivatives inhibit aldosterone production by reducing Ca2+ level below resting values.

AB - Sodium uptake by rat adrenal glomerulosa cells was stimulated by intracellular acidosis evoked by Na2+-propionate. This process was inhibited by 5-(N,N-hexamethylene)amiloride (HMA), a known inhibitor of the Na+-H+ exchange. These experiments demonstrate the existence of the Na+-H+ exchange in glomerulosa cells. Although amiloride inhibited the angiotensin II- and adrenocorticotropic hormone (ACTH)-induced aldosterone response, HMA, a more specific inhibitor of Na+-H+ exchange, failed to do that. 45Ca2+ influx and efflux were dependent on intra- and extracellular Na+ concentrations. Amiloride analogues, known to inhibit Na+-Ca2+ exchange, reduced basal 45Ca influx. Although we could not reveal the activation of Na+-Ca2+ exchange by angiotensin II, inhibitors of Na-Ca2+ exchange also inhibited the angiotensin- and ACTH-induced aldosterone response of glomerulosa cells. Our results suggest that Na+-Ca2+ exchange supports the maintenance of basal Ca2+ level in the cytoplasma of glomerulosa cells, and amiloride derivatives inhibit aldosterone production by reducing Ca2+ level below resting values.

UR - http://www.scopus.com/inward/record.url?scp=0023878631&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0023878631&partnerID=8YFLogxK

M3 - Article

C2 - 2837093

AN - SCOPUS:0023878631

VL - 254

JO - American Journal of Physiology

JF - American Journal of Physiology

SN - 0363-6119

IS - 6

ER -