Renal sympathetic denervation raises blood pressure and attenuates ventricular remodeling in rats with myocardial infarction

Renal denervation (RDN) is reported to suppress the sympathetic nervous system and renin-angiotensin system, thereby, lowering blood pressure in patients with resistant hypertension. However, the effect and safety of RDN on ventricular remodeling following myocardial infarction (MI), especially with hypotension, is unknown. Forty rats were randomized into: MI, MI+RDN, Sham and RDN groups to examine the impact of RDN on blood pressure and ventricular remodeling in MI rats. Results: Compared with the MI group, MI+RDN showed lower levels of plasma norepinephrine, angiotensin II, cardiac angiotensin II, and angiotensin II type 1 receptor (P < 0.05). On days 21 and 28, there was a distinct increase of SBP in the MI+RDN group, compared with the MI group (P < 0.05). Compared with the MI group on days 14, 21 and 28, a significant increase of DBP in the MI+RDN group was observed (P < 0.05). RDN ameliorated decreases of ejection fraction and fractional shortening, as well as increases in left ventricular internal dimensions in MI rats (P < 0.05). RDN also caused decreases of collagen volume fraction in MI rats and inhibited the deposition of Collagens I and III, as well as the expression of transforming growth factor-beta 1 (TGF-beta 1) (P < 0.05). In conclusions, RDN raises blood pressure and improves post-infarction ventricular remodeling in MI rats, probably due to the suppression of TGF-beta 1 expression and collagen deposition via inhibition of SNS and RAS. RDN is a novel anti-fibrotic method for post-infarction remodeling and may be used in other cardiovascular diseases with similar pathological processes.