title: β2-Adrenoceptor agonists as potential therapeutic drugs in diabetic peripheral neuropathy.
abstract: OBJECTIVE
  the aim of the current study was to assess the effect of a β2-adrenoceptor agonist; namely salbutamol, on hyperalgesic as well as nerve dysfunction components of diabetic peripheral neuropathy.
  
  
  METHODS
  the present study was conducted on 60 male Wistar albino rats divided into six groups. Groups I and II were normal control rats injected by a single i.p. injection of normal saline and received 2% gum acacia (Group I) or salbutamol (Group II) for six weeks, starting one week following saline injection. Groups III-VI: rats that were rendered diabetic by a single i.p. injection of STZ and received either 2% gum acacia, salbutamol, salbutamol and propranolol or salbutamol and atenolol, respectively daily orally for six weeks, starting one week following STZ injection.
  
  
  RESULTS
  vehicle-treated diabetic rats exhibited: significant sciatic nerve dysfunction in the form of significantly prolonged distal latency and significantly decreased maximum peak and peak to peak amplitude of compound muscular action potential, significant thermal and mechanical hyperalgesia evidenced by significant decrease in hot plate latency, tail-flick latency and vocalization threshold, respectively. Salbutamol administration improved nerve dysfunction as well as thermal and mechanical hyperalgesia. These effects of salbutamol are most likely mediated by β2-adrenoceptors evidenced by significant abolishment of salbutamol effects after administration of the non-selective rather than the selective beta blockers; propranolol and atenolol, respectively.
  
  
  CONCLUSIONS
  chronic administration of salbutamol could ameliorate DPN, an effect which is most likely mediated by β2-adrenoceptors.
authors.affiliation: Clinical Pharmacology Department, Faculty of Medicine, Alexandria University, Egypt. Electronic address: azza.baraka@alexmed.edu.eg.
authors.forename: A M
authors.initials: AM
authors.lastname: Baraka
authors.affiliation: Clinical Pharmacology Department, Faculty of Medicine, Alexandria University, Egypt.
authors.forename: I E
authors.initials: IE
authors.lastname: Darwish
authors.affiliation: Clinical Pharmacology Department, Faculty of Medicine, Alexandria University, Egypt.
authors.forename: M T
authors.initials: MT
authors.lastname: Ghoneim
authors.affiliation: Physical Medicine Department, Faculty of Medicine, Alexandria University, Egypt.
authors.forename: H K
authors.initials: HK
authors.lastname: Korayem
mesh_terms: D058666:Adrenergic beta-2 Receptor Agonists / Q000494:pharmacology* / Q000627:therapeutic use; D000818:Animals; D003929:Diabetic Neuropathies / Q000139:chemically induced / Q000188:drug therapy* / Q000503:physiopathology; D055724:Electrophysiological Phenomena / Q000187:drug effects; D006930:Hyperalgesia / Q000188:drug therapy; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D018343:Receptors, Adrenergic, beta-2 / Q000378:metabolism*; D013311:Streptozocin / Q000009:adverse effects
chemical_list: D058666:Adrenergic beta-2 Receptor Agonists; D018343:Receptors, Adrenergic, beta-2; D013311:Streptozocin
keywords: Diabetes; Neuropathy; Salbutamol; Streptozotocin; β(2)-adrenoceptor agonists