| Summary: | Abstract Aims Some studies support the occurrence of nerve regeneration in renal arteries after renal denervation (RDN). But it is unclear whether inhibiting reinnervation after RDN is beneficial to enhancing the effect of RDN on chronic heart failure (CHF). Methods and results Chronic heart failure Sprague Dawley rats induced by transverse aortic constriction were administered with the analogue of Nogo‐B (Nogo group) or its antagonist (NEP group) respectively after RDN. Echocardiography, messenger RNA, and protein expression of calcitonin gene‐related peptide (CGRP) in renal artery and nerves surrounding renal artery were detected. Relative protein expression of CGRP was significantly decreased in the Nog group compared with the RDN group (0.64 ± 0.51 vs. 1.68 ± 1.07, P = 0.048). The number of nerves surrounding renal artery was higher in the NEP group than in the Nog group. Left ventricular end‐systolic volume and diameter (LVVs and LVDs) were greatly decreased, and left ventricular ejection fraction (LVEF) and fractional shortening (FS) increased significantly in the RDN, Nog and NEP groups when compared with the HF group (all P < 0.05). No significant differences were observed in left ventricular end‐diastolic volume and diameter; LVDs; LVVs; FS; LVEF; and the levels of plasma renin, noradrenaline, and N‐terminal pro‐B‐type natriuretic peptide among three groups: the RDN, Nog, and NEP groups. Conclusions Reinnervation of renal artery occurred in CHF rats after RDN, which had no effect on therapeutic role of RDN in CHF, and inhibiting this neural regeneration had no clinical significance and did not affect the efficacy of RDN to CHF.
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