“…A more likely explanation is that either the sensitivity of the cells synthesizing PGD 2 to BA and MN is increased or that the synthesis of PGD 2 in diabetes is enhanced. There is some evidence of increased synthesis observed in vas deferens and cardiac microsomes in diabetic rats [20,21]. As far as the role of other prostaglandins in the pathogenesis of diabetic complications is concerned, it is worth mentioning that the increased excretion of PGE 2 from the kidney of diabetic mice is connected with the renal vasodilatation and hyper®ltration seen in human diabetics [22].…”
“…A more likely explanation is that either the sensitivity of the cells synthesizing PGD 2 to BA and MN is increased or that the synthesis of PGD 2 in diabetes is enhanced. There is some evidence of increased synthesis observed in vas deferens and cardiac microsomes in diabetic rats [20,21]. As far as the role of other prostaglandins in the pathogenesis of diabetic complications is concerned, it is worth mentioning that the increased excretion of PGE 2 from the kidney of diabetic mice is connected with the renal vasodilatation and hyper®ltration seen in human diabetics [22].…”
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