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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

Acetylcholine-induced vasodilation in the perfused kidney of the streptozotocin-induced diabetic rat: role of prostacyclin.

Using the perfused kidneys of age-matched controls and streptozotocin (STZ)-induced diabetic rats, we previously demonstrated that endothelial dysfunction is present in STZ-induced diabetic rats and that acetylcholine (ACh) increases the level of 6-keto-prostaglandin F(1alpha) (a metabolite of prostacyclin) in the effluent from such perfused kidneys. Here, we investigated whether the ACh-induced relaxation in the perfused kidney is modulated by prostacyclin and/or thromboxane A(2) (TXA(2)) in the STZ-induced diabetic state. ACh-induced renal vasodilatation was significantly weaker in STZ-induced diabetic rats than in age-matched controls, and it was not affected by treatment with 10 muM furegrelate (TXA(2)-synthase inhibitor) or 1 muM SQ29548 (TXA(2)- receptor antagonist) in either group. However, it was attenuated by 10 muM tranylcypromine (prostacyclin-synthesis inhibitor), but only in the diabetic group. These results suggest that the endothelium-dependent relaxation induced by ACh in the renal vascular bed of STZ-induced diabetic rats is regulated by prostacyclin, not by TXA(2). Increased prostacyclin-signaling may occur to help compensate for the impaired endothelial function seen in the kidney in long-term diabetic states.[1]

References

  1. Acetylcholine-induced vasodilation in the perfused kidney of the streptozotocin-induced diabetic rat: role of prostacyclin. Kamata, K., Hosokawa, M., Matsumoto, T., Kobayashi, T. Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi (2006) [Pubmed]
 
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