Abstract: FR-PO213
Pathophysiological Analysis of Renal Congestion Using a Novel Rat Model
Session Information
- Vascular Biology and Dysfunction
November 03, 2017 | Location: Hall H, Morial Convention Center
Abstract Time: 10:00 AM - 10:00 AM
Category: Hypertension
- 1103 Vascular Biology and Dysfunction
Authors
- Shimada, Satoshi, Graduate School of Medicine, Tohoku University, Sendai, Japan
- Mori, Takefumi, TOHOKU MEDICAL AND PHARMACEUTICAL UNIVERSITY HOSPITAL, Sendai, Japan
- Ohsaki, Yusuke, Graduate School of Medicine, Tohoku University, Sendai, Japan
- Takahashi, Chika, Graduate School of Medicine, Tohoku University, Sendai, Japan
- Ito, Sadayoshi, Graduate School of Medicine, Tohoku University, Sendai, Japan
Background
A physiological association between kidney and heart has been well known, however the mechanisms involved is remain unknown. Renal congestion (RC) has been shown to play a role in heart failure (HF), precise mechanism involved in the pathogenesis of cardio-renal injury and Na retention has not been well investigated. The present study designed to investigate the role of renal congestion on glomerular filtration rate (GFR), renal histology, volume and blood pressure (BP).
Methods
RC was made by occluding left renal vein in Sprague Dawley rats. First, RC was made in left kidney while right kidney remained intact in anesthetized rats. GFR, renal interstitial hydrostatic pressure (RIHP) and urinary Na excretion was monitored in each kidney. Next, renal histology was compared between RC left kidney and intact right kidney after 9 days of RC. Finally, BP was monitored in rats with left RC with the other kidney removed. Rats were fed either normal salt or high salt for 2 weeks in either RC rats or sham operated rats.
Results
GFR and renal medullary blood flow significantly decreased in RC kidney while those of contralateral intact kidney remained unchanged. RIHP was increased during RC.
Tubulo-glomerular injury was observed in the RC left kidney compared to the contralateral intact right kidney. These renal injuries were improved by reducing RIHP with removing renal capsule. In one-kidney RC model, plasma renin activity (renal congestion group 5.6±0.7 ng/ml/h, n=13 vs sham group 10.1±0.8 ng/ml/h, n=9, p=0.011) and hematocrit (operation group 43.5±1.4 ng/ml/h, n=13 vs sham group 47.8±0.9 ng/ml/h, n=9, p=0.001) is significantly lower in RC group compared to those of sham group, which suggests the increase in volume of body fluid. High salt induced increase in systolic BP the one-kidney renal congestion rats (normal salt period 95.8±5.9mmHg vs high salt period 116.1±6.1 mmHg, n=7, p=0.013), while no significant changes in BP was observed in sham operated rats.
Conclusion
RC increases body fluid volume by Na retention and reduced GFR and renal circulation by increase in RIHP, thereby induce salt induced increase in BP and renal injury. These results indicate that renal congestion play a pathophysiological role in the pathogenesis of HF.
Funding
- Government Support - Non-U.S.