Abstract: FR-PO338
Renin-Angiotensin System Mediates Renal Vasoconstriction Induced by Acute Renal Venous Pressure Elevation in Rats
Session Information
- Hypertension and CVD: Mechanisms - I
October 26, 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
- Huang, Xiaohua, University of Alberta, Edmonton, Alberta, Canada
- Hamza, Shereen M., University of Alberta, Edmonton, Alberta, Canada
- Zhuang, Wenqing, Univ. of Alberta, Edmonton, Alberta, Canada
- Cupples, William A., Simon Fraser University, Burnaby, British Columbia, Canada
- Braam, Branko, University of Alberta, Edmonton, Alberta, Canada
Background
Combined cardiac/renal dysfunction is characterized by elevated renal venous pressure (RVP). Renin-angiotensin system (RAS) is presumably an important mediator of worsening kidney function at a high RVP. In the present study, our hypothesis is that acute RVP elevation increases vascular tone leading to decreased renal vascular conductance (RVC) can be abolished when endogenous angiotensin II (ANG II) is inhibited. Our objective is to evaluate RVP induced renal hemodynamic response during ANG II inhibition.
Methods
Male Lewis rats (350-450g) received a regular sodium diet were randomized as time control or subjected to RVP increase to 20 mmHg. EndogenousANG II was blocked using Enalapril infusion and mean arterial pressure (MAP) was restored by continuous, constant ANG II (ANG II “clamped”, n=18) or vasopressin (AVP)(n=11) infusion.To increase RVP, the left renal vein was partially occluded for 120 min following 60 min baseline. MAP, renal blood flow (RBF) and GFR were continuously monitored.
Results
When ANG II was clamped, elevating RVP (0.4±0.3 to 19.6±0.3 mmHg) induced a reduction of MAP by experiment end (Δ -22±4 mmHg, P<0.05). The RVP-induced RVC reduction previously observed in intact rats was completely inhibited(Δ 0.011±0.005 ml/min. mmHg). ANG II clamp did not prevent the decrease of both RBF (Δ -1.9±0.4ml/min, P<0.05), and ipsilateral GFR (Δ -0.77±0.18 ml/min, P<0.05). In AVP-infused animals, RVP increase (0.1±0.4 to 19.6±0.6 mmHg) did not impact MAP (Δ -5.6±4.0 mmHg). Although RBF decreased (Δ -1.3±0.7ml/min, P<0.05), RVC did not decrease (Δ 0.022±0.011 ml/min. mmHg) and the reduction of GFR was attenuated (Δ -0.45±0.15 ml/min).
Conclusion
RVP induced renal vasoconstriction was abolished and reduction in RBF and GFR was attenuated when ANG II was fixed or inhibited. This suggests a primary role for the RAS in the vasoconstriction induced by increased RVP.