The Influence of Inhibiting Renal Neural Regeneration on the Efficacy of Renal Denervation to Chronic Heart Failure

Figures

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  Figure 1. The animal grouping and time line of the experimental protocol. Sprague Dawley rats, 10 weeks of age, were subjected to transverse aortic constriction (TAC). Then renal denervation (RDN) was performed at the 20th week (the 10th week after TAC) after echocardiography. At the 28th week (the 8th week after RDN), the rats underwent RDN were administered with Nogo‐P4 (the analogue of Nogo‐B), NEP1‐40 (the antagonist of Nogo‐B) or saline water by intraperitoneal injection respectively. At the 46th week, echocardiography was performed, and blood samples and renal arteries tissues were harvested for analysis.

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  Figure 2. Comparisons of plasma parameters and mRNA expression of indicator of nerve regeneration in the renal arteries among the five groups. The levels of plasma renin (A), noradrenaline (B), Nog‐B (C), N‐terminal pro‐B‐type natriuretic peptide (NT‐proBNP) (D) and the ratio of heart to body weight (E) in the control, heart failure (HF), renal denervation (RDN), Nog and NEP groups. The relative mRNA levels of calcitonin gene‐related peptide (CGRP) (F), nerve growth factor (β‐NGF) (G), and growth‐associated protein 43 (GAP‐43) (H). * P < 0.05 vs. the HF and #P < 0.05 vs. the RDN group.

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  Figure 3. Levels of plasma and echocardiographic parameters in the different groups. The levels of plasma renin (A), noradrenaline (B), Nog‐B (C), N‐terminal pro‐B‐type natriuretic peptide (NT‐proBNP) (D), left ventricular end‐systolic diameter (LVDs) and end‐diastolic diameter (LVDd) (E), left ventricular end‐systolic volume (LVVs) and end‐diastolic volume (LVVd) (F), fractional shortening (FS) and left ventricular ejection fraction (LVEF) (G), and LV mass and LV mass corrected (H) in the Control 1, Control 2, Control 3, HF 1, HF 2, and HF 3 groups. *P < 0.05 vs. the Control 2 group.

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  Figure 4. The protein expression of calcitonin gene‐related peptide (CGRP), nerve growth factor (β‐NGF) and growth‐associated protein 43 (GAP‐43) in the renal arteries in the different groups. Western blot analysis of CGRP, GAP‐43 and β‐NGF expression in the control (A), heart failure (HF) (B), renal denervation (RDN) (C), Nog (D) and NEP (E) groups and relative mRNA levels of CGRP (F), β‐NGF (G), and GAP‐43 (H) in the renal arteries in the different groups. *P < 0.05 vs. the HF and # P < 0.05 vs. the RDN group.

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  Figure 5. Difference of echocardiographic parameters among the control, heart failure (HF), renal denervation (RDN), Nog, and NEP groups at 4 months after administration. Comparison of left ventricular end‐systolic diameter (LVDs), left ventricular end‐diastolic diameter (LVDd) (A), left ventricular end‐systolic volume (LVVs), left ventricular end‐diastolic volume (LVVd) (B), fractional shortening (FS), left ventricular ejection fraction (LVEF) (C), and LV mass and LV mass corrected (D) among the control, HF, RDN, Nog, and NEP groups. Representative echocardiographic images in the HF (E), RDN (F), Nog (G), and NEP (H) rats. *P < 0.05 vs. HF and # P < 0.05 vs. RDN group.

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  Figure 6. Haematoxylin and eosin staining and immunohistochemistry of calcitonin gene‐related peptide (CGRP) in the renal artery tissues in different groups. Haematoxylin and eosin staining of the renal artery in the heart failure (HF) (A), renal denervation (RDN) (B), Nog (C) and NEP (D) groups and immunohistochemistry of CGRP in the HF (E), RDN (F), Nog (G), and NEP (H) groups. Semi‐quantitative analysis of CGRP levels by measuring integrated optical density (IOD) (E). *P < 0.05 vs. HF and # P < 0.05 vs. RDN group.