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Fig. 1 | BMC Cardiovascular Disorders

Fig. 1

From: Role of peroxisome proliferators-activated receptor-gamma in advanced glycation end product-mediated functional loss of voltage-gated potassium channel in rat coronary arteries

Fig. 1

Role of PPAR-γ in AGE-induced impairment of Kv channel-mediated dilation in RSCAs. a The first top record of tension indicated that 1 μM or 10 μM acetylcholine (arrows) failed to dilate denuded arteries while 10 μM Forskolin (dot) normally dilated the arteries. The other typical records showed concentration-dependent dilation to Forskolin in endothelium-denuded coronary arteries incubated with control vehicle (HEPES solution), 200 μg/mL BSA, 200 μg/mL AGE, 200 μg/mL AGE+ 1 mM ALA, 200 μg/mL AGE+ 0.1 mM PIO, or 200 μg/mL AGE+ 0.1 mM PIO + 0.1 mM GW9662 for 2 h. Arteries were precontracted with 1 μM U46619. Dots indicate Forskolin concentration from 10− 10 to 10− 5 M. b-e Cumulative concentration-response curves showing Forskolin-induced general dilation (b, d) and Kv channel-mediated dilation (c, e) in endothelium-denuded RSCAs. The Kv channel-mediated dilation was defined as the difference between dilations measured before and after incubation with 3 mM 4-aminopyridine (4-AP) for 30 min. n = 6 vessels per group. * P < 0.05 vs. BSA; # P < 0.05 vs. AGE; § P < 0.05 vs. AGE + PIO

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