Diabetes-induced enhancement of prostanoid-stimulated contraction in mesenteric veins of mice.
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We investigated the influence of the diabetic state on the contractile response of longitudinal segments of isolated mesenteric vein to prostanoids and leukotriene (LT), and the contribution of the vascular endothelium to modulation of the contractile response was determined. The normal mesenteric vein and deendothelialized veins of normal (ddY), diabetic KK-CA<SUP>y</SUP> and streptozotocin ddY mice (150 mg/kg, i.v., 6 weeks) were used. In the diabetic state, the contractions produced by noradrendline (60 μM), high K<SUP>+</SUP> solution (143.4 mM), and the thromboxane A<SUB>2</SUB> analogue U-4661 9 (29 nM-29 mM) were not affected, and LTD<SUB>4</SUB> (0.1 nM-1 μM)-induced contraction was suppressed. Contractions induced by prostaglandin (PG) E<SUB>2</SUB> (0.2 μM-2 mM), PGF<SUB>2α</SUB> (0.3 μM-0.3 mM) and the prostacyclin derivatives PGI<SUB>2</SUB>-Na (10-100 μM) and TRK-100 (0.2 μM-2mM) were significantly enhanced in the presence of an intact vascular endothelium, but not in de-endothelialized segments. The increase in PGF<SUB>2α</SUB> (0.28 mM) contractions was dependent on age (correlation coefficient r=0.36, significant difference, P<0.05) and blood glucose (r=0.88, significant difference, P<0.01), but was independent of obesity. The contractile response to PGD<SUB>2</SUB> (0.3-0.9 mM) was enhanced in both intact and de-endothelialized segments. These results indicate that the diabetic state affects prostanoid responses in an endothelium-dependent manner, except for the PGD<SUB>2</SUB> response, which is independent of the endothelium.
- 公益社団法人 日本薬理学会の論文
公益社団法人 日本薬理学会 | 論文
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