Abstract P248: Changes in Dipping Pattern of Blood Pressure During the Progression of Renal Injury in Dahl Salt-sensitive Hypertensive Rats
A growing body of clinical evidence has indicated that non-dipper pattern of circadian rhythm of blood pressure (BP) is a great risk of cardiovascular disease, which is accompanied by impaired renal function and proteinuria. Here, we aimed to investigate the circadian rhythm of BP during the progression of renal injury in Dahl salt-sensitive (DSS) hypertensive rats. DSS rats were treated with a high salt diet (HS; 8% NaCl) for 10 weeks (n=10). Before starting a HS diet, the difference in mean arterial pressure (MAP) between dark and light period was 6.46±0.61 mmHg in normal salt (0.3% NaCl)-fed DSS rats. Treatment with a HS diet for 5 days did not change renal function, but blood pressure was increased. Furthermore, the difference in MAP between dark and light period was significantly increased (11.05±0.87 mmHg, P<0.05), suggesting extreme dipping type of circadian BP. However, further HS diet feeding for 10 weeks induced the development of hypertension, renal tissue injury and proteinuria, which were associated with non-dipper pattern of BP. Namely, the MAP was similar between dark and light period (180.47±6.26 vs.177.92±6.33 mmHg). After switching to normal salt diet for 4 weeks, MAP was significantly decreased and circadian rhythm of BP was returned to normal dipper type (157.27±3.96 vs. 149.93±4.11 for MAP in dark and light period, respectively). In conclusion, the present study has demonstrated that treatment with HS diet initially showed extreme dipping pattern of BP in DSS rats, whereas it changed to non-dipping pattern of BP during the progression of renal tissue injury and proteinuria. These data support the hypothesis that non-dipping pattern of BP is associated with the progression of renal injury during the development of salt-dependent hypertension, which may contribute to the cardiovascular events.
Author Disclosures: A. Nishiyama: B. Research Grant (includes principal investigator, collaborator, or consultant and pending grants as well as grants already received); Modest; Collaborative studies or research grants; Daiichi-Sankyo Co. Ltd., Novartis Co. Ltd., Taisho-Toyama Pharm. Co. Ltd., Chu-gai Pharm. Co., Ltd., Ajinomoto Pharm. Co., Ltd., Mochida Pharma. Co., Ltd.. C. Other Research Support (includes receipt of drugs, supplies, equipment or other in-kind support); Modest; Drug compounds were provided by Ajinomoto Pharm. Co. Ltd., Daiichi-Sankyo Co. Ltd., Novartis A.G., Taisho-Toyama Pharm. Co. Ltd., Boehringer-Ingelheim Co., Ltd.. D. Speaker (includes speakers bureau, symposia, and expert witness); Modest; Mochida Pharm. Co. Ltd., Daiichi-Sankyo Co. Ltd., Taisho-Toyama Pharm. Co. Ltd., Boehringer-Ingelheim Co., Ltd., Pfizer Co., Ltd., Novartis Co. Ltd.. Y. Fujisawa: None. A. Rahman: None. A. Rahman: None. D. Nakano: None. H. Hitomi: None. A. Sufiun: None.
- © 2015 by American Heart Association, Inc.