Comparison of vascular relaxation, lipolysis and glucose uptake by peroxisome proliferator-activated receptor-γ activation in +db/+m and +db/+db mice

Pioglitazone, a Peroxisome Proliferator–Activated Receptor-γ Agonist, Induces Dilation of Isolated Porcine Retinal Arterioles: Role of Nitric Oxide and Potassium Channels

“…Animal studies to examine the effects of pioglitazone on vascular responses in the aorta have reported conflicting results as to whether pioglitazone causes endothelium-dependent 38 or -independent vasodilation, 39 or both. 35 In the present study, we first observed that the removal of the vascular endothelium by CHAPS, which we confirmed with immunohistochemical staining (Fig.…”

“…NO involvement in pioglitazone-induced vasodilation was also reported in isolated rat 35 and mouse aortas. 38 Collectively, it is reasonable that NO contributes greatly to the endotheliumdependent component of pioglitazone-induced vasodilation in the retinal microcirculation. In contrast to L-NAME, the vasodilatory response to pioglitazone was unaffected by inhibition of synthesis of prostacyclin or cytochrome P450 metabolites, the other two vasodilators secreted from the endothelium (Fig.…”

Acute Simvastatin Inhibits KATP Channels of Porcine Coronary Artery Myocytes

“…[ 3 H]-2-Deoxy-glucose uptake into porcine coronary artery myocytes was determined using previously described protocols with minor modifications [30]. All experiments were performed in HEPES-buffered Ringer’s solution containing (mM): NaCl 135; KCl 5; NaH 2 PO 4 3.33; Na 2 HPO 4 0.83; CaCl 2 1.0; MgCl 2 1.0 and HEPES 5 (pH 7.4).…”

Folic acid consumption reduces resistin level and restores blunted acetylcholine-induced aortic relaxation in obese/diabetic mice

“…Inhibitors [N G -nitro-L-arginine methyl ester (L-NAME), resistin, LY 294002, geldanamycin and triciribine] were added to the organ bath 30 min before the administration of phenylephrine for active tone induction for the construction of the cumulative concentration-response curve by acetylcholine. The contractile force generated by phenylephrine was normalized to high K + (40 mM, which elicited similar magnitudes of aortic contraction in +db/+m and +db/+db mice) so as to adjust the concentration of phenylephrine (0.4-1 μM) used to elicit a comparable degree of contraction, as we have previously reported [2,27], under different conditions/manipulations (e.g., endothelium removal and addition of L-NAME, LY 294002, geldanamycin and triciribine) in both strains.…”

“…Thoracic aortas were dissected from animals immediately after sacrifice, and the isometric tension change of isolated aorta in response to drug challenge was measured, as previously described [2,26,27]. To exclude the involvement of cyclooxygenase and acetylcholinesterase, we included indomethacin (1 μM, a nonselective cyclooxygenase inhibitor) and neostigmine (10 μM, an acetylcholinesterase inhibitor) in the physiological salt solution throughout the experiments.…”