Effects of Glucagon-like Peptide-1 in Diabetic Rat Small Resistance Arteries

Bayram Z., NACİTARHAN C., ÖZDEM S. S.

JOURNAL OF CARDIOVASCULAR PHARMACOLOGY, cilt.64, sa.3, ss.277-284, 2014 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 64 Sayı: 3
  • Basım Tarihi: 2014
  • Doi Numarası: 10.1097/fjc.0000000000000120
  • Dergi Adı: JOURNAL OF CARDIOVASCULAR PHARMACOLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.277-284
  • Anahtar Kelimeler: diabetes mellitus, endothelium-derived hyperpolarizing factor, glucagon-like peptide-1, nitric oxide, potassium channels, resistance artery, ENDOTHELIAL DYSFUNCTION, DEPENDENT RELAXATION, OXIDATIVE STRESS, CONDUIT ARTERIES, BLOOD-PRESSURE, GLP-1, AMIDE, HYPERGLYCEMIA, RECEPTOR, INSULIN
  • Akdeniz Üniversitesi Adresli: Evet

Özet

We investigated the functional effects of glucagon-like peptide-1 [GLP-1(7-36)] and GLP-1(9-36) and the mechanism(s) playing a role in the effects of these agents in isolated small resistance arteries from control and diabetic rats. Cumulative concentrations of GLP-1(7-36) and GLP-1(9-36) produced concentration-dependent relaxations in endothelium-intact but not endothelium-denuded arteries that were significantly decreased in diabetic rats. GLP-1 receptor antagonist exendin(9-39) significantly inhibited responses to GLP-1 analogs. Nitric oxide/cyclic guanosine monophosphate pathway blockers, but not indomethacin, significantly decreased responses to GLP-1(7-36) or GLP-1(9-36) in control and diabetic rats. 4-Aminopyridine or glibenclamide incubation did not alter relaxations to GLP-1 analogs. GLP-1(7-36)- and GLP-1(9-36)-induced relaxations were blunted significantly and to similar extends by charybdotoxin and apamin combination in control and diabetic rats. Catalase did not affect, whereas superoxide dismutase (SOD) caused a significant increase in relaxations to GLP-1 analogs only in diabetic rats. We provided evidence about the relaxant effects of GLP-1(7-36) and GLP-1(9-36) in resistance arteries that were reduced in diabetic rats. Both calcium-activated potassium channels and endothelium played a major role in relaxations. Increment in certain reactive oxygen species and/or reduction in superoxide dismutase function might play a role in reduced relaxant responses of resistance arteries to GLP-1(7-36) and GLP-1(9-36) in diabetic rats.