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Göteborgs universitets publikationer

Parasympathetic nerve-evoked protein synthesis, mitotic activity and salivary secretion in the rat parotid gland and the dependence on NO-generation.

Författare och institution:
Shariel Sayardoust (-); Jörgen Ekström (Institutionen för neurovetenskap och fysiologi, sektionen för farmakologi)
Publicerad i:
Archives of oral biology, 51 ( 3 ) s. 189-97
Artikel, refereegranskad vetenskaplig
Sammanfattning (abstract):
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, 2mg/kg intravenous of each) in the absence or presence of atropine (2mg/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 N(w)propyl-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.
Ämne (baseras på Högskoleverkets indelning av forskningsämnen):
Klinisk medicin
Amylases, biosynthesis, Animals, Arginine, analogs & derivatives, pharmacology, Blood Pressure, physiology, Electric Stimulation, methods, Enzyme Inhibitors, pharmacology, Female, Mitosis, physiology, NG-Nitroarginine Methyl Ester, pharmacology, Nitric Oxide, biosynthesis, Nitric Oxide Synthase, antagonists & inhibitors, Organ Size, physiology, Parasympathetic Nervous System, metabolism, physiology, Parotid Gland, drug effects, metabolism, physiology, Protein Biosynthesis, physiology, Rats, Rats, Sprague-Dawley, Salivation, physiology
Postens nummer:
Posten skapad:
2013-03-01 13:27

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