Why the study?
Does STZ-induced diabetes impair endothelium-dependent vasorelaxation and NOS activity in rat aortic rings compared to healthy controls?
Does STZ-induced diabetes impair endothelium-dependent vasorelaxation and NOS activity in rat aortic rings compared to healthy controls?
This preclinical study demonstrates that decreased NOS activity and endothelial cell membrane disruption contribute to the endothelial dysfunction observed in diabetes.
Implicates NOS impairment in diabetic endothelial dysfunction; extends animal models but leaves open human therapeutic relevance.
Impaired endothelium-dependent relaxation of blood vessels is a common feature in diabetes, but the exact underlying mechanisms have not yet been clarified. In present study, endothelium-dependent vasorelaxation of aortic rings were evaluated in vitro in streptozotocin (STZ)-induced diabetic and age-matched control rats. Moreover, nitric oxide synthase (NOS) activity of aortic endothelial cells was assessed in both diabetic and healthy rats using histochemical staining for nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase activity. The results showed a significant decrease of endothelium-dependent relaxation in response to acetylcholine (ACh) in diabetic rings, compared with controls, that was accompanied by a remarkable attenuation of NOS activity in diabetic sections of rat aorta stained for NADPH-diaphorase. Furthermore, a membrane disruption of some endothelial cells was also observed in all diabetic sections. It can be concluded that a decrease in NOS activity together with a disruption of endothelial cell membrane play a major role in endothelial dysfunction observed in diabetes.
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Shafiei et al. (2003) studied this question.
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