Abstract: SA-PO776
Chronic, Combined Cardiac and Renal Dysfunction Exacerbates Renal Venous Pressure-Induced Suppression of Systemic Blood Pressure and Renal Function in Rats
Session Information
- CKD: Mechanisms - III
November 09, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: CKD (Non-Dialysis)
- 2103 CKD (Non-Dialysis): Mechanisms
Authors
- Hamza, Shereen M., University of Alberta, Edmonton, Alberta, Canada
- Zehra, Tayyaba, University of Alberta, Edmonton, Alberta, Canada
- Cupples, William A., Simon Fraser University, Burnaby, British Columbia, Canada
- Braam, Branko, University of Alberta, Edmonton, Alberta, Canada
Background
Coexisting cardiac/renal dysfunction may be perpetuated by increased renal venous pressure (RVP) in this condition. We previously showed that acute RVP elevation depresses renal blood flow (RBF), GFR and induces renal vasoconstriction in the absence of changes in blood pressure in healthy rats. We established a rodent model of combined cardiac/renal dysfunction and tested whether an acute, superimposed RVP elevation would impair cardiovascular stability, baseline renal perfusion and exacerbate renal dysfunction.
Methods
Male rats were subjected to 5/6 renal mass resection (Nx or Sham) and 6% high salt diet to induce renal dysfunction followed 7 weeks later by ligation of the left anterior descending coronary artery (CL or Sham). Four experimental groups were as follows: CL+Nx (n=11); Sham CL+Nx (n=9); CL+ Sham Nx (n=3); Sham Control (n=4). 8 weeks post-recovery, rats were anesthetized and subjected to an acute experiment whereupon mean arterial pressure (MAP), heart rate (HR), RVP, RBF and GFR were measured at baseline and during partial left renal vein occlusion to increase RVP to 20-25 mmHg for 120 min.
Results
Baseline MAP, HR, RBF and renal vascular conductance (RVC) were comparable between all experimental groups. Baseline GFR was significantly depressed in CL+Nx and Sham CL+Nx groups compared to Sham Control and CL+Sham Nx groups. Upon RVP increase, an early, rapid and pronounced reduction in MAP occurred in CL+Nx, Sham CL+Nx and CL+Sham Nx compared to Sham Control (p<0.001); MAP fell to the same extent in all groups at the end of the recording period. HR fell gradually with the increase in RVP in all experimental groups to the same extent. RVP increase exacerbated the reduction in RBF in CL+Nx compared to Sham Control (p<0.001) with intermediate responses in Sham CL+Nx and CL+Sham Nx groups. Similarly, RVP increase virtually eliminated GFR in CL+Nx (-99%), Sham CL+Nx (-95%) and CL+Sham Nx (-100%) groups compared to Sham Control (-82% from baseline; p<0.001). Renal vascular conductance dropped significantly but comparably upon RVP increase in all experimental groups.
Conclusion
Combined cardiac/renal dysfunction impairs cardiovascular stability in response to elevated RVP; MAP instability impairs the ability to maintain RBF and GFR considering preserved intrarenal responses.