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Nicotinic receptor agonist-induced salivation and its cellular mechanism in parotid acini of rats.
Auton Neurosci. 2011 Apr 26; 161(1-2):81-6.AN

Abstract

Cigarette smoking and nicotine enhance parotid saliva secretion, however, the underlying mechanism is unclear. To address the mechanism of nicotine-induced salivation and to explore the possibility that nicotinic receptor agonists act as sialogogues, we investigated the effects of nicotinic receptor agonists on salivary secretion in vivo and on intracellular Ca²+ concentration in digested parotid acini in vitro in rats. In urethane-anesthetized rats, intravenous administration of nicotinic receptor agonists, nicotine and cytisine, at 3 μmol/kg increased whole saliva output accompanied by a pressor response with nicotine, but not with cytisine. Using Ca²+-imaging system on digested parotid acini in which autonomic nerve terminals were kept intact, nicotine and cytisine dose-dependently increased intracellular Ca²+ concentration at μM level. This was not observed in single acinar cells containing no nerve terminal. The nicotine-induced Ca²+ response was largely blocked by a muscarinic receptor antagonist and partly blocked by an adrenergic receptor antagonist. Furthermore, the same nicotine-induced Ca²+ response was blocked by mecamylamine, a relatively selective nicotinic antagonist for α3β4 subtype receptor, but not by other selective antagonists, dihydro-β-erythroidine for α4-containing receptor and methyllycaconitine for α7 nicotinic receptors. These results suggest that nicotinic agonists-induced salivation is due to a release of acetylcholine and noradrenaline from autonomic nerve terminals through activation of α3β4 nicotinic receptor subtype. In addition, considering the blood pressure response and development of addiction with nicotine, cytisine may be a better therapeutic candidate to serve as a sialogogue for xerostomia patients.

Authors+Show Affiliations

Department of Biosciences, Kyushu Dental College, 2-6-1 Manazuru, Kokurakitaku, Kitakyushu, Fukuoka 803-8580, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

21300575

Citation

Iida, Taichi, et al. "Nicotinic Receptor Agonist-induced Salivation and Its Cellular Mechanism in Parotid Acini of Rats." Autonomic Neuroscience : Basic & Clinical, vol. 161, no. 1-2, 2011, pp. 81-6.
Iida T, Ono K, Inagaki T, et al. Nicotinic receptor agonist-induced salivation and its cellular mechanism in parotid acini of rats. Auton Neurosci. 2011;161(1-2):81-6.
Iida, T., Ono, K., Inagaki, T., Hosokawa, R., & Inenaga, K. (2011). Nicotinic receptor agonist-induced salivation and its cellular mechanism in parotid acini of rats. Autonomic Neuroscience : Basic & Clinical, 161(1-2), 81-6. https://doi.org/10.1016/j.autneu.2011.01.003
Iida T, et al. Nicotinic Receptor Agonist-induced Salivation and Its Cellular Mechanism in Parotid Acini of Rats. Auton Neurosci. 2011 Apr 26;161(1-2):81-6. PubMed PMID: 21300575.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Nicotinic receptor agonist-induced salivation and its cellular mechanism in parotid acini of rats. AU - Iida,Taichi, AU - Ono,Kentaro, AU - Inagaki,Tomohiro, AU - Hosokawa,Ryuji, AU - Inenaga,Kiyotoshi, PY - 2010/10/26/received PY - 2010/12/13/revised PY - 2011/01/12/accepted PY - 2011/2/9/entrez PY - 2011/2/9/pubmed PY - 2011/8/6/medline SP - 81 EP - 6 JF - Autonomic neuroscience : basic & clinical JO - Auton Neurosci VL - 161 IS - 1-2 N2 - Cigarette smoking and nicotine enhance parotid saliva secretion, however, the underlying mechanism is unclear. To address the mechanism of nicotine-induced salivation and to explore the possibility that nicotinic receptor agonists act as sialogogues, we investigated the effects of nicotinic receptor agonists on salivary secretion in vivo and on intracellular Ca²+ concentration in digested parotid acini in vitro in rats. In urethane-anesthetized rats, intravenous administration of nicotinic receptor agonists, nicotine and cytisine, at 3 μmol/kg increased whole saliva output accompanied by a pressor response with nicotine, but not with cytisine. Using Ca²+-imaging system on digested parotid acini in which autonomic nerve terminals were kept intact, nicotine and cytisine dose-dependently increased intracellular Ca²+ concentration at μM level. This was not observed in single acinar cells containing no nerve terminal. The nicotine-induced Ca²+ response was largely blocked by a muscarinic receptor antagonist and partly blocked by an adrenergic receptor antagonist. Furthermore, the same nicotine-induced Ca²+ response was blocked by mecamylamine, a relatively selective nicotinic antagonist for α3β4 subtype receptor, but not by other selective antagonists, dihydro-β-erythroidine for α4-containing receptor and methyllycaconitine for α7 nicotinic receptors. These results suggest that nicotinic agonists-induced salivation is due to a release of acetylcholine and noradrenaline from autonomic nerve terminals through activation of α3β4 nicotinic receptor subtype. In addition, considering the blood pressure response and development of addiction with nicotine, cytisine may be a better therapeutic candidate to serve as a sialogogue for xerostomia patients. SN - 1872-7484 UR - https://www.unboundmedicine.com/medline/citation/21300575/Nicotinic_receptor_agonist_induced_salivation_and_its_cellular_mechanism_in_parotid_acini_of_rats_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1566-0702(11)00005-1 DB - PRIME DP - Unbound Medicine ER -