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Secretagogue-induced RVD in HSY cells is due to K+ channels activated by Ca2+ and protein kinase C
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| Zeitschriftentitel: | American Journal of Physiology-Cell Physiology |
|---|---|
| Personen und Körperschaften: | , |
| In: | American Journal of Physiology-Cell Physiology, 265, 1993, 5, S. C1405-C1411 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
American Physiological Society
|
| Schlagwörter: |
| author_facet |
Moran, A. Turner, R. J. Moran, A. Turner, R. J. |
|---|---|
| author |
Moran, A. Turner, R. J. |
| spellingShingle |
Moran, A. Turner, R. J. American Journal of Physiology-Cell Physiology Secretagogue-induced RVD in HSY cells is due to K+ channels activated by Ca2+ and protein kinase C Cell Biology Physiology |
| author_sort |
moran, a. |
| spelling |
Moran, A. Turner, R. J. 0363-6143 1522-1563 American Physiological Society Cell Biology Physiology http://dx.doi.org/10.1152/ajpcell.1993.265.5.c1405 <jats:p>To maintain cell volume, absorptive epithelia must coordinate ion fluxes associated with transcellular transport with those required for volume regulation. K+ channels are thought to play a central regulatory role in this process. Electronic cell sizing was used to study the regulatory volume decrease (RVD) response of the human salivary ductal cell line HSY. Following a hypotonic challenge, RVD was markedly enhanced by the muscarinic agonist carbachol (half-maximal effect approximately 1.4 microM). Carbachol-induced RVD was mimicked by the K+ ionophore valinomycin and inhibited by K+ channel blockers, indicating that it is due to the activation of K+ channels. Carbachol-induced RVD was blocked by maneuvers that blunted the carbachol-induced rise in intracellular Ca2+ concentration ([Ca2+]i) and mimicked by ionomycin-induced increases in [Ca2+]i, but concentrations of ionomycin (100 nM) yielding [Ca2+]i well above carbachol-induced levels were required. However, when treatment with 2.5 nM ionomycin, which produced [Ca2+]i in the carbachol-generated range, was combined with treatment with low concentrations of an active phorbol ester, an enhancement of RVD similar to that observed with carbachol alone was observed. These data provide strong evidence that carbachol-induced RVD in the HSY cells involves K+ channels that are tightly regulated by both [Ca2+]i and protein kinase C.</jats:p> Secretagogue-induced RVD in HSY cells is due to K+ channels activated by Ca2+ and protein kinase C American Journal of Physiology-Cell Physiology |
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10.1152/ajpcell.1993.265.5.c1405 |
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American Physiological Society, 1993 |
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American Physiological Society, 1993 |
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0363-6143 1522-1563 |
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1993 |
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American Journal of Physiology-Cell Physiology |
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49 |
| title |
Secretagogue-induced RVD in HSY cells is due to K+ channels activated by Ca2+ and protein kinase C |
| title_unstemmed |
Secretagogue-induced RVD in HSY cells is due to K+ channels activated by Ca2+ and protein kinase C |
| title_full |
Secretagogue-induced RVD in HSY cells is due to K+ channels activated by Ca2+ and protein kinase C |
| title_fullStr |
Secretagogue-induced RVD in HSY cells is due to K+ channels activated by Ca2+ and protein kinase C |
| title_full_unstemmed |
Secretagogue-induced RVD in HSY cells is due to K+ channels activated by Ca2+ and protein kinase C |
| title_short |
Secretagogue-induced RVD in HSY cells is due to K+ channels activated by Ca2+ and protein kinase C |
| title_sort |
secretagogue-induced rvd in hsy cells is due to k+ channels activated by ca2+ and protein kinase c |
| topic |
Cell Biology Physiology |
| url |
http://dx.doi.org/10.1152/ajpcell.1993.265.5.c1405 |
| publishDate |
1993 |
| physical |
C1405-C1411 |
| description |
<jats:p>To maintain cell volume, absorptive epithelia must coordinate ion fluxes associated with transcellular transport with those required for volume regulation. K+ channels are thought to play a central regulatory role in this process. Electronic cell sizing was used to study the regulatory volume decrease (RVD) response of the human salivary ductal cell line HSY. Following a hypotonic challenge, RVD was markedly enhanced by the muscarinic agonist carbachol (half-maximal effect approximately 1.4 microM). Carbachol-induced RVD was mimicked by the K+ ionophore valinomycin and inhibited by K+ channel blockers, indicating that it is due to the activation of K+ channels. Carbachol-induced RVD was blocked by maneuvers that blunted the carbachol-induced rise in intracellular Ca2+ concentration ([Ca2+]i) and mimicked by ionomycin-induced increases in [Ca2+]i, but concentrations of ionomycin (100 nM) yielding [Ca2+]i well above carbachol-induced levels were required. However, when treatment with 2.5 nM ionomycin, which produced [Ca2+]i in the carbachol-generated range, was combined with treatment with low concentrations of an active phorbol ester, an enhancement of RVD similar to that observed with carbachol alone was observed. These data provide strong evidence that carbachol-induced RVD in the HSY cells involves K+ channels that are tightly regulated by both [Ca2+]i and protein kinase C.</jats:p> |
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| author | Moran, A., Turner, R. J. |
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| author_sort | moran, a. |
| container_issue | 5 |
| container_start_page | 0 |
| container_title | American Journal of Physiology-Cell Physiology |
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| description | <jats:p>To maintain cell volume, absorptive epithelia must coordinate ion fluxes associated with transcellular transport with those required for volume regulation. K+ channels are thought to play a central regulatory role in this process. Electronic cell sizing was used to study the regulatory volume decrease (RVD) response of the human salivary ductal cell line HSY. Following a hypotonic challenge, RVD was markedly enhanced by the muscarinic agonist carbachol (half-maximal effect approximately 1.4 microM). Carbachol-induced RVD was mimicked by the K+ ionophore valinomycin and inhibited by K+ channel blockers, indicating that it is due to the activation of K+ channels. Carbachol-induced RVD was blocked by maneuvers that blunted the carbachol-induced rise in intracellular Ca2+ concentration ([Ca2+]i) and mimicked by ionomycin-induced increases in [Ca2+]i, but concentrations of ionomycin (100 nM) yielding [Ca2+]i well above carbachol-induced levels were required. However, when treatment with 2.5 nM ionomycin, which produced [Ca2+]i in the carbachol-generated range, was combined with treatment with low concentrations of an active phorbol ester, an enhancement of RVD similar to that observed with carbachol alone was observed. These data provide strong evidence that carbachol-induced RVD in the HSY cells involves K+ channels that are tightly regulated by both [Ca2+]i and protein kinase C.</jats:p> |
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| imprint_str_mv | American Physiological Society, 1993 |
| institution | DE-D275, DE-Bn3, DE-Brt1, DE-D161, DE-Gla1, DE-Zi4, DE-15, DE-Pl11, DE-Rs1, DE-14, DE-Ch1, DE-L229 |
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| series | American Journal of Physiology-Cell Physiology |
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| spelling | Moran, A. Turner, R. J. 0363-6143 1522-1563 American Physiological Society Cell Biology Physiology http://dx.doi.org/10.1152/ajpcell.1993.265.5.c1405 <jats:p>To maintain cell volume, absorptive epithelia must coordinate ion fluxes associated with transcellular transport with those required for volume regulation. K+ channels are thought to play a central regulatory role in this process. Electronic cell sizing was used to study the regulatory volume decrease (RVD) response of the human salivary ductal cell line HSY. Following a hypotonic challenge, RVD was markedly enhanced by the muscarinic agonist carbachol (half-maximal effect approximately 1.4 microM). Carbachol-induced RVD was mimicked by the K+ ionophore valinomycin and inhibited by K+ channel blockers, indicating that it is due to the activation of K+ channels. Carbachol-induced RVD was blocked by maneuvers that blunted the carbachol-induced rise in intracellular Ca2+ concentration ([Ca2+]i) and mimicked by ionomycin-induced increases in [Ca2+]i, but concentrations of ionomycin (100 nM) yielding [Ca2+]i well above carbachol-induced levels were required. However, when treatment with 2.5 nM ionomycin, which produced [Ca2+]i in the carbachol-generated range, was combined with treatment with low concentrations of an active phorbol ester, an enhancement of RVD similar to that observed with carbachol alone was observed. These data provide strong evidence that carbachol-induced RVD in the HSY cells involves K+ channels that are tightly regulated by both [Ca2+]i and protein kinase C.</jats:p> Secretagogue-induced RVD in HSY cells is due to K+ channels activated by Ca2+ and protein kinase C American Journal of Physiology-Cell Physiology |
| spellingShingle | Moran, A., Turner, R. J., American Journal of Physiology-Cell Physiology, Secretagogue-induced RVD in HSY cells is due to K+ channels activated by Ca2+ and protein kinase C, Cell Biology, Physiology |
| title | Secretagogue-induced RVD in HSY cells is due to K+ channels activated by Ca2+ and protein kinase C |
| title_full | Secretagogue-induced RVD in HSY cells is due to K+ channels activated by Ca2+ and protein kinase C |
| title_fullStr | Secretagogue-induced RVD in HSY cells is due to K+ channels activated by Ca2+ and protein kinase C |
| title_full_unstemmed | Secretagogue-induced RVD in HSY cells is due to K+ channels activated by Ca2+ and protein kinase C |
| title_short | Secretagogue-induced RVD in HSY cells is due to K+ channels activated by Ca2+ and protein kinase C |
| title_sort | secretagogue-induced rvd in hsy cells is due to k+ channels activated by ca2+ and protein kinase c |
| title_unstemmed | Secretagogue-induced RVD in HSY cells is due to K+ channels activated by Ca2+ and protein kinase C |
| topic | Cell Biology, Physiology |
| url | http://dx.doi.org/10.1152/ajpcell.1993.265.5.c1405 |