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Evidence that nitric oxide does not directly contribute to methacholine-induced amylase secretion in rabbit parotid acinar cells

  • Exocrine Glands
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Abstract

Nitric oxide (NO) is a short-lived free radical and is a widespread intra- and intercellular messenger molecule involved in various physiological functions. We have demonstrated previously that the muscarinic agonist methacholine induces endogenous generation of NO in rabbit parotid acinar cells. Since methacholine also simultaneously evokes amylase secretion, we investigated the effect of NO on the methacholine-induced exocytotic amylase secretion in rabbit parotid acinar cells. Methacholine-evoked amylase secretion was clearly reduced in the absence of extracellular Ca2+. The Ca2+-mobilizing reagents A23187 and thapsigargin, which stimulate NO generation, also evoked amylase secretion. This response seemed to be caused by NO generated by the activation of endogenous Ca2+-regulated NO synthase. However, N G-nitro-l-arginine methyl ester (L-NAME), a specific NOS inhibitor, and the NO scavenger haemoglobin had no effect on methacholine-induced amylase secretion. The NO generator sodium nitroprusside (SNP) failed to evoke amylase release. We further studied the effects of L-NAME and SNP on methacholine-induced amylase secretion in crudely dispersed parotid gland cell clusters containing nerve tissue. In this preparation, L-NAME inhibited methacholine-induced amylase secretion and SNP evoked amylase secretion. It is thus unlikely that NO contributes directly to methacholine-induced amylase secretion in rabbit parotid acinar cells. NO appears rather to affect to nerve tissues in the cell suspension.

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Acknowledgements

This study was supported in part by the Grant-in Aid for Scientific Research (No. 13470396) from the Ministry of Education, Sciences and Culture of Japan, by a Grant from the Ministry of Education, Culture, Sports, Science, and Technology to prompt multi-disciplinary research projects and by Nihon University Research Grant 2001-2002.

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Authors and Affiliations

  1. Department of Physiology, Nihon University School of Dentistry at Matsudo, Chiba 271-8587, Matsudo, Japan

    Shoji Tsunoda, Hiromi Michikawa, Shunsuke Furuyama & Hiroshi Sugiya

  2. Research Institute of Oral Science, Nihon University School of Dentistry at Matsudo, Chiba 271-8587, Matsudo, Japan

    Hiromi Michikawa, Shunsuke Furuyama & Hiroshi Sugiya

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  1. Shoji Tsunoda
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  2. Hiromi Michikawa
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  3. Shunsuke Furuyama
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  4. Hiroshi Sugiya
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Correspondence to Hiroshi Sugiya.

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Tsunoda, S., Michikawa, H., Furuyama, S. et al. Evidence that nitric oxide does not directly contribute to methacholine-induced amylase secretion in rabbit parotid acinar cells. Pflugers Arch - Eur J Physiol 446, 470–474 (2003). https://doi.org/10.1007/s00424-003-1055-6

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  • DOI: https://doi.org/10.1007/s00424-003-1055-6

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