title: Reduced muscarinic parotid secretion is underlain by impaired NO signaling in diabetic rabbits.
abstract: OBJECTIVE
  The influence of experimental diabetes (alloxan, 100 mg kg(-1) ) was studied on rabbit parotid gland function.
  
  
  METHODS
  Carbachol-induced parotid secretion in vivo, and in vitro quantification of inducible nitric oxide synthase (iNOS) mRNA expression, by real-time RT-PCR, and activity of superoxide dismutase (SOD) and total antioxidant capacity (TAC) in commercial colorimetric assays were measured in parotid glands of non-diabetic and diabetic rabbits.
  
  
  RESULTS
  Carbachol-induced dose-dependent increase in parotid secretion significantly reduced in diabetic rabbits. Functional studies in the presence of muscarinic receptor and nitric oxide synthase (NOS) antagonists revealed that in M3 receptor-mediated carbachol secretion, nitric oxide, deriving mainly from neuronal NOS (nNOS) in control, and iNOS in diabetic rabbits, was involved. Also, upregulation of iNOS mRNA expression and enhanced SOD activity and TAC were detected in diabetic glands.
  
  
  CONCLUSIONS
  Our data suggest that decreased M3 receptor-mediated parotid secretion in diabetic rabbits appears to be due to alterations in NO signaling, mainly due to iNOS induction, accompanied by elevated antioxidant response.
authors.affiliation: Department of Pharmacology in Dentistry, School of Dental medicine, University of Belgrade, Belgrade, Serbia.
authors.forename: J
authors.initials: J
authors.lastname: Roganović
authors.affiliation: Department of Pharmacology in Dentistry, School of Dental medicine, University of Belgrade, Belgrade, Serbia.
authors.forename: L J
authors.initials: LJ
authors.lastname: Djukić
authors.affiliation: Department of Physiology, School of Dental medicine, University of Belgrade, Belgrade, Serbia.
authors.forename: E
authors.initials: E
authors.lastname: Kršljak
authors.affiliation: Department of Neurobiology, Institute for Biological Research 'Siniša Stanković', University of Belgrade, Belgrade, Serbia.
authors.forename: N
authors.initials: N
authors.lastname: Tanić
authors.affiliation: Department of Pharmacology in Dentistry, School of Dental medicine, University of Belgrade, Belgrade, Serbia.
authors.forename: D
authors.initials: D
authors.lastname: Stojić
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D002217:Carbachol / Q000494:pharmacology; D018678:Cholinergic Agents / Q000494:pharmacology; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism; D052248:Nitric Oxide Synthase Type I / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000096:biosynthesis / Q000235:genetics / Q000378:metabolism; D010306:Parotid Gland / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology*; D012333:RNA, Messenger / Q000096:biosynthesis; D011817:Rabbits; D060888:Real-Time Polymerase Chain Reaction / Q000379:methods; D043587:Receptor, Muscarinic M3 / Q000037:antagonists & inhibitors / Q000378:metabolism*; D015398:Signal Transduction; D013482:Superoxide Dismutase / Q000378:metabolism; D015854:Up-Regulation
chemical_list: D000975:Antioxidants; D018678:Cholinergic Agents; D012333:RNA, Messenger; D043587:Receptor, Muscarinic M3; D009569:Nitric Oxide; D002217:Carbachol; D019001:Nitric Oxide Synthase; D052248:Nitric Oxide Synthase Type I; D052247:Nitric Oxide Synthase Type II; D013482:Superoxide Dismutase
keywords: diabetes; inducible nitric oxide synthase; oxidative stress; parotid secretion