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Voltage-gated calcium currents have two opposing effects on the secretion of aldosterone
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| Zeitschriftentitel: | American Journal of Physiology-Cell Physiology |
|---|---|
| Personen und Körperschaften: | , , , , |
| In: | American Journal of Physiology-Cell Physiology, 268, 1995, 4, S. C985-C992 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
American Physiological Society
|
| Schlagwörter: |
| author_facet |
Barrett, P. Q. Ertel, E. A. Smith, M. M. Nee, J. J. Cohen, C. J. Barrett, P. Q. Ertel, E. A. Smith, M. M. Nee, J. J. Cohen, C. J. |
|---|---|
| author |
Barrett, P. Q. Ertel, E. A. Smith, M. M. Nee, J. J. Cohen, C. J. |
| spellingShingle |
Barrett, P. Q. Ertel, E. A. Smith, M. M. Nee, J. J. Cohen, C. J. American Journal of Physiology-Cell Physiology Voltage-gated calcium currents have two opposing effects on the secretion of aldosterone Cell Biology Physiology |
| author_sort |
barrett, p. q. |
| spelling |
Barrett, P. Q. Ertel, E. A. Smith, M. M. Nee, J. J. Cohen, C. J. 0363-6143 1522-1563 American Physiological Society Cell Biology Physiology http://dx.doi.org/10.1152/ajpcell.1995.268.4.c985 <jats:p>Using Ca2+ channel blockers with different specificities for L- and T-type Ca2+ channels, we have investigated the roles of these two channel types in K(+)-induced aldosterone secretion. In whole cell voltage-clamp experiments, the spider toxin omega-agatoxin-IIIA (omega-Aga-IIIA) completely blocks L-type Ca2+ channels but has no effect on T-type Ca2+ channels. In contrast, Ni2+ and 1,4-dihydropyridines block both L- and T-type Ca2+ channels. Secretion induced by 7 mM extracellular K+ concentration ([K+]o) is unaffected by omega-Aga-IIIA but is strongly inhibited by Ni2+ or the 1,4-dihydropyridine, nitrendipine. This suggests that physiological increases in [K+]o stimulate aldosterone secretion primarily by enhancing Ca2+ entry through T-type Ca2+ channels. Surprisingly, secretion induced by 60 mM [K+]o is enhanced by omega-Aga-IIIA or Ni2+ and is inhibited by the L-type Ca2+ channel activator BAY K 8644. Nitrendipine (1 nM) also stimulates such secretion, although higher concentrations are inhibitory (concentration inhibiting 50% of maximal response approximately 30 nM). If extracellular Ca2+ concentration is reduced from 1.25 to 0.5 mM, secretion induced by 60 mM [K+]o is enhanced, and Ni2+ or low nitrendipine become inhibitory. Together, these results that L-type Ca2+ currents can reduce steroidogenesis and that the role of these currents was previously misconstrued because 1,4-dihydropyridines modify secretion by multiple mechanisms. Thus Ca2+ entry can function as a negative modulator of steroid secretion.</jats:p> Voltage-gated calcium currents have two opposing effects on the secretion of aldosterone American Journal of Physiology-Cell Physiology |
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1995 |
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American Journal of Physiology-Cell Physiology |
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49 |
| title |
Voltage-gated calcium currents have two opposing effects on the secretion of aldosterone |
| title_unstemmed |
Voltage-gated calcium currents have two opposing effects on the secretion of aldosterone |
| title_full |
Voltage-gated calcium currents have two opposing effects on the secretion of aldosterone |
| title_fullStr |
Voltage-gated calcium currents have two opposing effects on the secretion of aldosterone |
| title_full_unstemmed |
Voltage-gated calcium currents have two opposing effects on the secretion of aldosterone |
| title_short |
Voltage-gated calcium currents have two opposing effects on the secretion of aldosterone |
| title_sort |
voltage-gated calcium currents have two opposing effects on the secretion of aldosterone |
| topic |
Cell Biology Physiology |
| url |
http://dx.doi.org/10.1152/ajpcell.1995.268.4.c985 |
| publishDate |
1995 |
| physical |
C985-C992 |
| description |
<jats:p>Using Ca2+ channel blockers with different specificities for L- and T-type Ca2+ channels, we have investigated the roles of these two channel types in K(+)-induced aldosterone secretion. In whole cell voltage-clamp experiments, the spider toxin omega-agatoxin-IIIA (omega-Aga-IIIA) completely blocks L-type Ca2+ channels but has no effect on T-type Ca2+ channels. In contrast, Ni2+ and 1,4-dihydropyridines block both L- and T-type Ca2+ channels. Secretion induced by 7 mM extracellular K+ concentration ([K+]o) is unaffected by omega-Aga-IIIA but is strongly inhibited by Ni2+ or the 1,4-dihydropyridine, nitrendipine. This suggests that physiological increases in [K+]o stimulate aldosterone secretion primarily by enhancing Ca2+ entry through T-type Ca2+ channels. Surprisingly, secretion induced by 60 mM [K+]o is enhanced by omega-Aga-IIIA or Ni2+ and is inhibited by the L-type Ca2+ channel activator BAY K 8644. Nitrendipine (1 nM) also stimulates such secretion, although higher concentrations are inhibitory (concentration inhibiting 50% of maximal response approximately 30 nM). If extracellular Ca2+ concentration is reduced from 1.25 to 0.5 mM, secretion induced by 60 mM [K+]o is enhanced, and Ni2+ or low nitrendipine become inhibitory. Together, these results that L-type Ca2+ currents can reduce steroidogenesis and that the role of these currents was previously misconstrued because 1,4-dihydropyridines modify secretion by multiple mechanisms. Thus Ca2+ entry can function as a negative modulator of steroid secretion.</jats:p> |
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| author | Barrett, P. Q., Ertel, E. A., Smith, M. M., Nee, J. J., Cohen, C. J. |
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| description | <jats:p>Using Ca2+ channel blockers with different specificities for L- and T-type Ca2+ channels, we have investigated the roles of these two channel types in K(+)-induced aldosterone secretion. In whole cell voltage-clamp experiments, the spider toxin omega-agatoxin-IIIA (omega-Aga-IIIA) completely blocks L-type Ca2+ channels but has no effect on T-type Ca2+ channels. In contrast, Ni2+ and 1,4-dihydropyridines block both L- and T-type Ca2+ channels. Secretion induced by 7 mM extracellular K+ concentration ([K+]o) is unaffected by omega-Aga-IIIA but is strongly inhibited by Ni2+ or the 1,4-dihydropyridine, nitrendipine. This suggests that physiological increases in [K+]o stimulate aldosterone secretion primarily by enhancing Ca2+ entry through T-type Ca2+ channels. Surprisingly, secretion induced by 60 mM [K+]o is enhanced by omega-Aga-IIIA or Ni2+ and is inhibited by the L-type Ca2+ channel activator BAY K 8644. Nitrendipine (1 nM) also stimulates such secretion, although higher concentrations are inhibitory (concentration inhibiting 50% of maximal response approximately 30 nM). If extracellular Ca2+ concentration is reduced from 1.25 to 0.5 mM, secretion induced by 60 mM [K+]o is enhanced, and Ni2+ or low nitrendipine become inhibitory. Together, these results that L-type Ca2+ currents can reduce steroidogenesis and that the role of these currents was previously misconstrued because 1,4-dihydropyridines modify secretion by multiple mechanisms. Thus Ca2+ entry can function as a negative modulator of steroid secretion.</jats:p> |
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| spelling | Barrett, P. Q. Ertel, E. A. Smith, M. M. Nee, J. J. Cohen, C. J. 0363-6143 1522-1563 American Physiological Society Cell Biology Physiology http://dx.doi.org/10.1152/ajpcell.1995.268.4.c985 <jats:p>Using Ca2+ channel blockers with different specificities for L- and T-type Ca2+ channels, we have investigated the roles of these two channel types in K(+)-induced aldosterone secretion. In whole cell voltage-clamp experiments, the spider toxin omega-agatoxin-IIIA (omega-Aga-IIIA) completely blocks L-type Ca2+ channels but has no effect on T-type Ca2+ channels. In contrast, Ni2+ and 1,4-dihydropyridines block both L- and T-type Ca2+ channels. Secretion induced by 7 mM extracellular K+ concentration ([K+]o) is unaffected by omega-Aga-IIIA but is strongly inhibited by Ni2+ or the 1,4-dihydropyridine, nitrendipine. This suggests that physiological increases in [K+]o stimulate aldosterone secretion primarily by enhancing Ca2+ entry through T-type Ca2+ channels. Surprisingly, secretion induced by 60 mM [K+]o is enhanced by omega-Aga-IIIA or Ni2+ and is inhibited by the L-type Ca2+ channel activator BAY K 8644. Nitrendipine (1 nM) also stimulates such secretion, although higher concentrations are inhibitory (concentration inhibiting 50% of maximal response approximately 30 nM). If extracellular Ca2+ concentration is reduced from 1.25 to 0.5 mM, secretion induced by 60 mM [K+]o is enhanced, and Ni2+ or low nitrendipine become inhibitory. Together, these results that L-type Ca2+ currents can reduce steroidogenesis and that the role of these currents was previously misconstrued because 1,4-dihydropyridines modify secretion by multiple mechanisms. Thus Ca2+ entry can function as a negative modulator of steroid secretion.</jats:p> Voltage-gated calcium currents have two opposing effects on the secretion of aldosterone American Journal of Physiology-Cell Physiology |
| spellingShingle | Barrett, P. Q., Ertel, E. A., Smith, M. M., Nee, J. J., Cohen, C. J., American Journal of Physiology-Cell Physiology, Voltage-gated calcium currents have two opposing effects on the secretion of aldosterone, Cell Biology, Physiology |
| title | Voltage-gated calcium currents have two opposing effects on the secretion of aldosterone |
| title_full | Voltage-gated calcium currents have two opposing effects on the secretion of aldosterone |
| title_fullStr | Voltage-gated calcium currents have two opposing effects on the secretion of aldosterone |
| title_full_unstemmed | Voltage-gated calcium currents have two opposing effects on the secretion of aldosterone |
| title_short | Voltage-gated calcium currents have two opposing effects on the secretion of aldosterone |
| title_sort | voltage-gated calcium currents have two opposing effects on the secretion of aldosterone |
| title_unstemmed | Voltage-gated calcium currents have two opposing effects on the secretion of aldosterone |
| topic | Cell Biology, Physiology |
| url | http://dx.doi.org/10.1152/ajpcell.1995.268.4.c985 |