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Parasympathetic nerve-evoked protein synthesis, mitotic activity and salivary secretion in the rat parotid gland and the dependence on NO-generation
Department of Pharmacology, Sahlgrenska Academy Göteborg University, Göteborg, Sweden.
Department of Pharmacology, Sahlgrenska Academy at Göteborg University, Göteborg, Sweden.
2006 (English)In: Archives of Oral Biology, ISSN 0003-9969, E-ISSN 1879-1506, Vol. 51, no 3, p. 189-197Article in journal (Refereed) Published
Abstract [en]

Incorporation of radiolabelled leucine and thymidine into trichloroacetic acid-insoluble material of the parotid gland was used as indices of protein synthesis and mitotic activity, respectively, following electrical stimulation of the parasympathetic auriculo-temporal nerve for 30 min in pentobarbitone-anaesthetized rats under adrenoceptor blockade (phentolamine and propranolol, 2 mg/kg intravenous of each) in the absence or presence of atropine (2 mg/kg intravenous) and without or with nitric oxide synthase inhibitors. In atropinized rats, the parasympathetic non-adrenergic, non-cholinergic (NANC) nerve-evoked mean increases in protein synthesis at a frequency of 10 Hz (142%) and 40 Hz (200%) were not affected in a statistically significant way (124 and 275%, respectively) by the neuronal type NO-synthase inhibitor Nwpropyl-l-arginine (N-PLA) (30 mg/kg intravenous). Neither were the increase (175%) in protein synthesis at 10 Hz in non-atropinized animals affected by N-PLA (180%). The increase (65%) in mitotic activity, 19 h after the end of stimulation at 40 Hz, in the presence of atropine, was not affected by N-PLA (55%). Neither were the increase (95%) in gland content of amylase at this point of observation statistically significant affected by N-PLA (144%). The secretion of fluid and output of amylase from the parotid gland upon nerve stimulation was not affected by N-PLA. When examining the non-selective NO-synthase inhibitor L-NAME (30 mg/kg intravenous) in atropinized rats subjected to stimulation at 10 Hz, neither the increase in protein synthesis nor the evoked fluid response or amylase outputs were affected. Hence, in contrast to an NO-dependent sympathetic-induced protein synthesis and mitosis in the parotid gland, involving the activity of the neuronal type NO-synthase, no support for a parasympathetic-induced protein synthesis (and gain in gland amylase) and mitosis, depending on NO-generation, was found. Likewise, the present findings provide no evidence for a role of NO in the parasym pathetic nerve-evoked fluid secretion and amylase output. 

Place, publisher, year, edition, pages
Elsevier, 2006. Vol. 51, no 3, p. 189-197
Keywords [en]
Mitosis, Nitric oxide, Parasympathetic innervation, Parotid glands, Protein synthesis, Secretion, amylase, arginine, drug derivative, enzyme inhibitor, n(g) nitroarginine methyl ester, N(omega) propylarginine, N(omega)-propylarginine, nitric oxide synthase, animal, article, biosynthesis, blood pressure, cholinergic system, drug antagonism, drug effect, electrostimulation, female, metabolism, methodology, organ size, parotid gland, physiology, rat, salivation, Sprague Dawley rat, Amylases, Animals, Electric Stimulation, Enzyme Inhibitors, NG-Nitroarginine Methyl Ester, Parasympathetic Nervous System, Protein Biosynthesis, Rats, Rats, Sprague-Dawley, Animalia
National Category
Dentistry
Identifiers
URN: urn:nbn:se:hj:diva-45107DOI: 10.1016/j.archoralbio.2005.07.004ISI: 000235971100004PubMedID: 16144693Scopus ID: 2-s2.0-32944476944OAI: oai:DiVA.org:hj-45107DiVA, id: diva2:1330774
Available from: 2019-06-26 Created: 2019-06-26 Last updated: 2019-06-26Bibliographically approved

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