Abstract: SA-PO993
Chronic, Isolated Renal Venous Pressure Increase Induces Extensive Renal Venous Collateral Formation and Exacerbates Renal and Cardiovascular Dysfunction in Rats
Session Information
- Hypertension and CVD: Mechanisms - II
October 27, 2018 | Location: Exhibit Hall, San Diego Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Hypertension and CVD
- 1403 Hypertension and CVD: Mechanisms
Authors
- Hamza, Shereen M., University of Alberta, Edmonton, Alberta, Canada
- Huang, Xiaohua, University of Alberta, Edmonton, Alberta, Canada
- Zhuang, Wenqing, University of Alberta, Edmonton, Alberta, Canada
- Zehra, Tayyaba, University of Alberta, Edmonton, Alberta, Canada
- Lapierre, Morgan, 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). 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. Since physiological consequence of long-term, isolated RVP elevation are unknown, we tested whether chronic RVP elevation would impair baseline renal perfusion, exacerbating renal dysfunction and cardiovascular instability in response to superimposed acute RVP increase. Objectives: (1) Develop and characterize chronic, isolated RVP model (2) Evaluate baseline cardiovascular and renal response to chronic RVP elevation and superimposed acute increases in RVP.
Methods
Male rats were subjected to partial, graded occlusion of the left renal vein to induce chronic RVP elevation (20-25mmHg) and allowed to recover for either 1 (n=5) or 3 weeks (n=6). Rats were subsequently anesthetized and blood pressure, RVP, RBF and GFR were measured at baseline and during further RVP increase for 120 min.
Results
Chronic RVP elevation induced extensive renal venous collateral formation, evident within 1 week. This adaptation reduced RVP from 20-25 mmHg to 3.6±0.2 (1 wk) and 1.3±0.5 mmHg (3wk). Baseline blood pressure was unchanged by chronic RVP elevation (1 wk: 102±25; 3wk: 91±5 mmHg); however RBF and GFR were severely reduced at 1wk (RBF: 3.6±0.5 mL/min; GFR: 0.7±0.2 ml/min) and 3 wks (RBF: 3.1±1.2 mL/min). GFR was too low at 3 weeks to be reliably measured. Upon further RVP increase, blood pressure dropped in both 1 wk (-37±10 mmHg, p<0.05) and 3 wk groups (-19±1 mmHg, p<0.05). RBF also fell (1 wk: -2.3±0.7; 3wk: -1.3±0.6 mL/min, p<0.05), with reductions in renal vascular conductance (1 wk: -0.020±0.006; 3 wk: -0.010±0.007 mL/min.mmHg-1) and GFR (1wk: -0.56±0.14 mL/min).
Conclusion
Chronic RVP elevation elicits extensive renal venous collateral formation which alleviates venous congestion; however baseline renal function is suppressed. RVP-induced renal and cardiovascular dysfunction is exacerbated compared to our previous report of acute increase in RVP alone, thus long-term RVP elevation impairs critical mechanisms required to stabilize hemodynamics.