Role of (Na+)i and (Ca2+)i in nicotine-induced norepinephrine release from bovine adrenal chromaffin cells
Intracellular free sodium ([Na+]i) and calcium ([Ca2+]i) concentrations were determined by sodium-binding benzofuran isophthalate (SBFI) and fura 2 microfluorimetry, respectively, in bovine adrenal chromaffin cells (BCC). Validation of SBFI microfluorimetry by in vitro and in vivo calibration reveal...
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| Main Authors: | , , , , , |
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| Format: | Article (Journal) |
| Language: | English |
| Published: |
1 September 1995
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| In: |
American journal of physiology. Cell physiology
Year: 1995, Volume: 269, Issue: 3, Pages: C572-C581 |
| ISSN: | 1522-1563 |
| DOI: | 10.1152/ajpcell.1995.269.3.C572 |
| Online Access: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1152/ajpcell.1995.269.3.C572 Verlag, lizenzpflichtig, Volltext: https://journals.physiology.org/doi/abs/10.1152/ajpcell.1995.269.3.C572 
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| Author Notes: | Stefan H. Gerber, Armin Haunstetter, Carsten Krüger, Alexander Kaufmann, Rainer Nobiling, and Markus Haass |
| Summary: | Intracellular free sodium ([Na+]i) and calcium ([Ca2+]i) concentrations were determined by sodium-binding benzofuran isophthalate (SBFI) and fura 2 microfluorimetry, respectively, in bovine adrenal chromaffin cells (BCC). Validation of SBFI microfluorimetry by in vitro and in vivo calibration revealed a reliable assessment of [Na+]i within a range of 1-30 mM in single BCC. Nicotine (0.1-10 microM) induced concentration-dependent increases of both [Na+]i (from 3.3 +/- 0.1 to 25.6 +/- 0.4 mM, n = 76, P < 0.001) and [Ca2+]i (from 64 +/- 1 to 467 +/- 16 nM, n = 87, P < 0.001), which were accompanied by an increase in [3H]norepinephrine (NE) release. Consistent with an exocytotic release mechanism, nicotine-induced increments of [Ca2+]i and [3H]NE release were reduced under calcium-free conditions and by gadolinium chloride (40 microM), whereas [Na+]i was not affected. In contrast, a parallel attenuation of nicotine-evoked changes in [Na+]i, [Ca2+]i, and [3H]NE release was observed during reduction of the extracellular sodium concentration. The nicotine-evoked responses were neutralized by the nicotinic receptor antagonist hexamethonium (100 microM) but not by blockade of voltage-dependent sodium channels (1 microM tetrodotoxin). In conclusion, the nicotine-induced exocytotic release of [3H]NE is triggered by an increase in [Ca2+]i, which is facilitated by sodium influx through the nicotinic receptor ionophore. |
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| Item Description: | Gesehen am 12.05.2025 |
| Physical Description: | Online Resource |
| ISSN: | 1522-1563 |
| DOI: | 10.1152/ajpcell.1995.269.3.C572 |