Dasheng Lu1, Jingfeng Wang2, Hongxiang Zhang3, Qijun Shan4, Birong Zhou5. 1. Department of Cardiology, The Second Affiliated Hospital of Wannan Medical College, 10# Kangfu road, Wuhu 241000, Anhui Province, China; Vascular Diseases Research Center of Wannan Medical College, Wuhu 241000, China. Electronic address: wydslu@wnmc.edu.cn. 2. Department of Cardiology, The First Affiliated Hospital of Wannan Medical College, Wuhu 241000, China. 3. Department of Cardiology, The Second Affiliated Hospital of Wannan Medical College, 10# Kangfu road, Wuhu 241000, Anhui Province, China; Vascular Diseases Research Center of Wannan Medical College, Wuhu 241000, China. Electronic address: zhang_hxx@126.com. 4. Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, 300# Guangzhou road, Nanjing 210029, Jiangsu Province, China. 5. Department of Cardiology, The First Affiliated Hospital of Anhui Medical University, 218# Jixi road, Hefei 230032, Anhui Province, China. Electronic address: zhoubirong1@hotmail.com.
Abstract
AIMS: Investigate the effect of renal denervation (RDN) on chronic intermittent hypoxia (CIH) induced high blood pressure (BP) and cardiac injury, and explore whether the effect is associated with gut microbiota alteration and its product, trimethylamine N-oxide (TMAO). MATERIALS AND METHODS: Thirty six-week-old Sprague Dawley male rats were randomly divided into three groups: Control, CIH (20 cycles h-1, 7-8% at nadir, 8 h.day-1 for 6 weeks) and RDN group. Fecal samples, serum and heart tissue were collected at week 6. 16S rRNA gene sequencing was performed in fecal samples. KEY FINDINGS: Systolic BP in CIH group was significantly elevated compared with Control (164 ± 3 vs. 143 ± 4 mmHg, p = 0.004), while RDN treatment evidently reduced elevated systolic BP (133 ± 5 vs. 164 ± 3 mmHg, p < 0.001). CIH group featured significant cardiac perivascular fibrosis, compared with Control, whereas RDN treatment effectively attenuated perivascular fibrosis. Principal component analysis showed that CIH rats, but not RDN group were noticeably separated from Control. At phyla level, the structure of the biological community of RDN rats converged with that of control rats, which was apparently different in comparison to CIH rats. TMAO levels in the three groups were not significantly different. SIGNIFICANCE: RDN exerts beneficial effect on BP control and perivascular fibrosis in rats exposed to CIH. This effect is associated with its ability to revert the already skewed gut microbiota caused by CIH, but is not via regulation of TMAO.
AIMS: Investigate the effect of renal denervation (RDN) on chronic intermittent hypoxia (CIH) induced high blood pressure (BP) and cardiac injury, and explore whether the effect is associated with gut microbiota alteration and its product, trimethylamine N-oxide (TMAO). MATERIALS AND METHODS: Thirty six-week-old Sprague Dawley male rats were randomly divided into three groups: Control, CIH (20 cycles h-1, 7-8% at nadir, 8 h.day-1 for 6 weeks) and RDN group. Fecal samples, serum and heart tissue were collected at week 6. 16S rRNA gene sequencing was performed in fecal samples. KEY FINDINGS: Systolic BP in CIH group was significantly elevated compared with Control (164 ± 3 vs. 143 ± 4 mmHg, p = 0.004), while RDN treatment evidently reduced elevated systolic BP (133 ± 5 vs. 164 ± 3 mmHg, p < 0.001). CIH group featured significant cardiac perivascular fibrosis, compared with Control, whereas RDN treatment effectively attenuated perivascular fibrosis. Principal component analysis showed that CIHrats, but not RDN group were noticeably separated from Control. At phyla level, the structure of the biological community of RDN rats converged with that of control rats, which was apparently different in comparison to CIHrats. TMAO levels in the three groups were not significantly different. SIGNIFICANCE: RDN exerts beneficial effect on BP control and perivascular fibrosis in rats exposed to CIH. This effect is associated with its ability to revert the already skewed gut microbiota caused by CIH, but is not via regulation of TMAO.