Preservation of CGRP in myocardium attenuates development of cardiac dysfunction in diabetic rats

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• 作者：Tao Sun^a ; ¹ ; Zheng Guo^a ; ^b ; ^c ; ¹ ; ^{guozheng713@163.com" class="auth_mail" title="E-mail the corresponding author} ; Chao-Jie Liu^a ; ¹ ; Mu-Rong Li^a ; ¹ ; Tu-Ping Li^a ; ¹ ; Xin Wang^a ; ¹ ; Da-Jiang Yuan^a
• 关键词：Cardiac dysfunction ; TRPV1 ; Calcitonin gene-related peptide ; CGRP ; Diabetes
• 刊名：International Journal of Cardiology
• 出版年：2016
• 出版时间：1 October 2016
• 年：2016
• 卷：220
• 期：Complete
• 页码：226-234
• 全文大小：1300 K

文摘

Calcitonin gene-related peptide (CGRP) plays an important role in cardiovascular regulation, which was found reduced in serum of diabetic patients. To test the hypothesis that lack of CGRP in myocardium is associated with diabetic cardiac dysfunction, which may be improved by preservation of CGRP in diabetic rats.

Methods and results

Diabetes was induced in male Sprague–Dawley rats by streptozotocin (50 mg/kg). Two groups of the diabetic rats, one fed with standard laboratory chew and another with the laboratory food plus hot pepper (containing 0.0174% of capsaicin), to stimulate production and release of CGRP. Cardiac functions were evaluated by measurements of intraventricular pressures after 8 weeks of development of diabetes. Transient receptor potential vanilloid type 1 (TRPV1), CGRP, β1-adreneregic receptor and norepinephrine were analyzed. Significantly lower levels of TRPV1 and CGRP were detected in the thoracic dorsal root ganglia (DRG) and myocardium of the diabetic animals, along with significant decline in left ventricular systolic pressure (by 24%) and heart rate (by 25%) and increase of the end-diastolic pressure (by 83%) with obvious reduction of CGRP in the DRG, by 41%, the myocardium (by 30%) and the serum (by 20%). The cardiac performance, the TRPV1 and the CGRP in the diabetic animals fed with hot pepper were well preserved. No any significant change in β1-adreneregic receptor and norepinephrine was detected.

Conclusion

The findings may suggest a novel mechanism underlying diabetic cardiac dysfunctions via impairing TRPV1-CGRP pathway in myocardium. Preservation of the TRPV1-CGRP mechanism may prevent the development of cardiac dysfunction in diabetes.