کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5810422 1556552 2016 5 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Could angiotensin-(1-7) be connected with improvement of microvascular function in diabetic patients? Angiotensin-(1-7) iontophoresis may provide the answer
ترجمه فارسی عنوان
آیا ممکن است آنژیوتانسین- (1-7) با بهبود عملکرد میکروواسکولار در بیماران دیابتی مرتبط باشد؟ یونوفروزیس آنژیوتانسین (1-7) ممکن است جواب دهد
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شناسی تکاملی
چکیده انگلیسی

Diabetes mellitus, a metabolic disorder with significant global health care burden, causes chronic microvascular and macrovascular complications that still comprise a therapeutic challenge. Angiotensin-(1-7), a heptapeptide with vasodilatory properties, has been found to restore vascular reactivity and endothelial cell function, mostly in experiments on larger isolated animal vessels and in cell cultures. The presented hypothesis suggests that angiotensin-(1-7) might have beneficial effects on microvascular function that is damaged in diabetic patients, alleviating endothelial dysfunction and increasing microvascular reactivity to various vasoactive agents in diabetes. It is further proposed that iontophoresis with angiotensin-(1-7) might be used to explore this potential beneficial effect, as well as provide a possible future therapeutic delivery method for angiotensin-(1-7). Since other peptides and proteins have been previously tested and used in iontophoretic transdermal delivery, it is plausible that angiotensin-(1-7) would be a suitable candidate for transdermal iontophoretic application for research (and potentially therapeutic) purposes. If confirmed, the delineated hypothesis would have immense implications for more effective care of diabetic patients, as well as for better understanding of microcirculatory pathophysiological mechanisms in diabetes.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Medical Hypotheses - Volume 93, August 2016, Pages 16-20
نویسندگان
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