| Online-Ressource |
Verfasst von: | Gerber, Stefan Horst [VerfasserIn]  |
| Haunstetter, Armin [VerfasserIn]  |
| Krüger, Carsten [VerfasserIn]  |
| Kaufmann, Alexander [VerfasserIn]  |
| Nobiling, Rainer [VerfasserIn]  |
| Haass, Markus [VerfasserIn]  |
Titel: | Role of (Na+)i and (Ca2+)i in nicotine-induced norepinephrine release from bovine adrenal chromaffin cells |
Verf.angabe: | Stefan H. Gerber, Armin Haunstetter, Carsten Krüger, Alexander Kaufmann, Rainer Nobiling, and Markus Haass |
E-Jahr: | 1995 |
Jahr: | 1 September 1995 |
Umfang: | 10 S. |
Fussnoten: | Gesehen am 12.05.2025 |
Titel Quelle: | Enthalten in: American journal of physiology. Cell physiology |
Ort Quelle: | Bethesda, Md. : American Physiological Society, 1977 |
Jahr Quelle: | 1995 |
Band/Heft Quelle: | 269(1995), 3, Seite C572-C581 |
ISSN Quelle: | 1522-1563 |
Abstract: | 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. |
DOI: | doi:10.1152/ajpcell.1995.269.3.C572 |
URL: | Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.
Volltext: https://doi.org/10.1152/ajpcell.1995.269.3.C572 |
| Volltext: https://journals.physiology.org/doi/abs/10.1152/ajpcell.1995.269.3.C572 |
| DOI: https://doi.org/10.1152/ajpcell.1995.269.3.C572 |
Datenträger: | Online-Ressource |
Sprache: | eng |
K10plus-PPN: | 1925306550 |
Verknüpfungen: | → Zeitschrift |
Role of (Na+)i and (Ca2+)i in nicotine-induced norepinephrine release from bovine adrenal chromaffin cells / Gerber, Stefan Horst [VerfasserIn]; 1 September 1995 (Online-Ressource)