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Methylglyoxal Impairs β 2-Adrenoceptor-Mediated Vasodilatory Mechanisms in Rat Retinal Arterioles

Methylglyoxal Impairs β 2-Adrenoceptor-Mediated Vasodilatory Mechanisms in Rat Retinal Arterioles

Mari Akagawa, Asami Mori, Kenji Sakamoto, Tsutomu Nakahara

Biol Pharm Bull. 2018;41(2):272-276.

PMID: 29386487

Abstract:

Methylglyoxal, a highly reactive dicarbonyl compound, is formed as a by-product of glycolysis and plays an important role in the pathogenesis of diabetic complications, including diabetic retinopathy. However, it remains to be determined how methylglyoxal affects the regulatory mechanisms of retinal blood flow. In this study, we examined the effects of methylglyoxal on β2-adrenoceptor-mediated vasodilatory mechanisms in rat retinal arterioles. The retinal vasodilator responses were assessed by measuring the diameter of retinal arterioles in the fundus images. Intravitreal injection of methylglyoxal significantly diminished the vasodilation of retinal arterioles induced by the β2-adrenoceptor agonist salbutamol. The vasodilator effect of BMS-191011, a large-conductance Ca2+-activated K+ (BKCa) channel opener, on retinal arterioles was also attenuated by methylglyoxal. In contrast, methylglyoxal had no significant effect on retinal vasodilator response to forskolin. Methylglyoxal attenuated retinal vasodilator response to salbutamol under blockade of BKCa channels with iberiotoxin, an inhibitor of the channels. These results suggest that methylglyoxal attenuates β2-adrenoceptor-mediated retinal vasodilation by impairing the coupling of the β2-adrenoceptor to the guanine nucleotide-binding protein (Gs protein) and the function of the BKCa channel. Increased methylglyoxal in the eyes may contribute to the impairment of regulatory mechanisms of retinal blood flow in patients with diabetic retinopathy.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP202821816	BMS-191011		202821-81-6	Price

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