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Verfasst von:Gerber, Stefan Horst [VerfasserIn]   i
 Haunstetter, Armin [VerfasserIn]   i
 Krüger, Carsten [VerfasserIn]   i
 Kaufmann, Alexander [VerfasserIn]   i
 Nobiling, Rainer [VerfasserIn]   i
 Haass, Markus [VerfasserIn]   i
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
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