Nitric Oxide Modulates a Late Step of Exocytosis

The effects of nitric oxide (NO) on the late phase of exocytosis have been studied, by amperometry, on Ba 2+ -stimulated chromaffin cells. Acute incubation with NO or NO donors (sodium nitroprusside, spermine-NO, S -nitrosoglutathione) produced a drastic slowdown of the granule emptying. Conversely,...

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Bibliographic Details
Published in:The Journal of biological chemistry 2000-07, Vol.275 (27), p.20274-20279
Main Authors: Machado, J D, Segura, F, Brioso, M A, Borges, R
Format: Article
Language:English
Subjects:
1-Methyl-3-isobutylxanthine - pharmacology
Animals
Barium - pharmacology
Catecholamines - metabolism
Cattle
Chromaffin Cells - drug effects
Chromaffin Granules - drug effects
Chromaffin Granules - metabolism
Cyclic GMP - analogs & derivatives
Cyclic GMP - pharmacology
Electrochemistry
Exocytosis - drug effects
Kinetics
NG-Nitroarginine Methyl Ester - pharmacology
Nitric Oxide - pharmacology
Nitroprusside
Nitroso Compounds - pharmacology
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Summary:The effects of nitric oxide (NO) on the late phase of exocytosis have been studied, by amperometry, on Ba 2+ -stimulated chromaffin cells. Acute incubation with NO or NO donors (sodium nitroprusside, spermine-NO, S -nitrosoglutathione) produced a drastic slowdown of the granule emptying. Conversely, cell treatment with N ω -nitro- l -arginine methyl ester (a NO synthase inhibitor) or with NO scavengers (methylene blue, 2-(4-carboxyphenyl)-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxide potassium) accelerated the extrusion of catecholamines from chromaffin granules, suggesting the presence of a NO modulatory tone. The incubation with phosphodiesterase inhibitors (3-isobutyl-1-methylxanthine or zaprinast) or with the cell-permeant cGMP analog 8-bromo-cGMP, mimicked the effects of NO, suggesting the involvement of the guanylate cyclase cascade. NO effects were not related to changes in intracellular Ba 2+ . NO did not modify the duration of feet. Effects were evident even on pre-fusioned granules, observed under hypertonic conditions, suggesting that the fusion pore is not the target for NO, which probably acts by modifying the affinity of catecholamines for the intragranular matrix. NO could modify the synaptic transmitter efficacy through a novel mechanism, which involves the regulation of the emptying of secretory vesicles.
ISSN:0021-9258
1083-351X
DOI:10.1074/jbc.M000930200