title: [Effects of clonidine on myocardial Gs alpha mRNA expression after scalds in rats].
abstract: OBJECTIVE
  To explore the role of clonidine (Clo) on myocardial Gs alpha mRNA expression after scalds in rats.
  
  
  METHODS
  A 30% skin-full-thickness scald was produced by immersing rats in 95 degrees C water for 10 s. The myocardial Gs alpha mRNA expression level, cyclic AMP content and adenylyl cyclase (AC) activity were determined with dot blotting hybridization, in situ hybridization, radioimmunoassay and indirect method.
  
  
  RESULTS
  Three hours after scalds, the myocardial Gs alpha mRNA was significantly decreased to (61 +/- 20)% of the control group (P < 0.01). AC activity and cAMP content were also decreased. Clo (0.3, 1.0 and 3.0 mg.kg-1, i.p.) was shown to increase myocardial Gs alpha mRNA expression level (P < 0.01 or P < 0.05) after scalds to (131 +/- 28)%, (142 +/- 51)% and (139 +/- 48)% of the scald group, respectively, which were correlated with the Clo dose (gamma = 0.597, P < 0.05). Clo 1.0 mg.kg-1 and 3.0 mg.kg-1 (i.p.) promoted AC activity and increased cAMP content, but Clo 0.3 and 0.1 mg.kg-1 showed no significant effect (P > 0.05). Selective I1-imidazoline receptor antagonist efaroxan (Efa) (10, 5 mg.kg-1, i.p.) was found to partially reverse the effect of Clo, while Efa 2.5 mg.kg-1 showed no significantly influence. The reduced quantity of Gs alpha mRNA expression level correlated well with the Efa dose (gamma = 0.900, P < 0.05). The change of AC and cAMP was similar to Gs alpha mRNA.
  
  
  CONCLUSIONS
  Clo increased the myocardial Gs alpha mRNA expression, AC activity and cAMP content after scalds in rats.
authors.affiliation: Department of Pharmacology, Third Military Medical University, Chongqing 400038, China. hg2@mail.tmmu.com.cn
authors.forename: Hai-gang
authors.initials: HG
authors.lastname: Zhang
authors.forename: Xiao-hui
authors.initials: XH
authors.lastname: Li
mesh_terms: D000262:Adenylyl Cyclases / Q000378:metabolism; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000818:Animals; D002056:Burns / Q000378:metabolism*; D003000:Clonidine / Q000494:pharmacology*; D000242:Cyclic AMP / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D019205:GTP-Binding Protein alpha Subunits, Gs / Q000096:biosynthesis* / Q000235:genetics; D015870:Gene Expression / Q000187:drug effects; D006321:Heart / Q000187:drug effects*; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D012333:RNA, Messenger / Q000096:biosynthesis / Q000187:drug effects; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar
chemical_list: D000318:Adrenergic beta-Agonists; D012333:RNA, Messenger; D000242:Cyclic AMP; D019205:GTP-Binding Protein alpha Subunits, Gs; D000262:Adenylyl Cyclases; D003000:Clonidine