Abstract: SA-PO391

Acute Renal Venous Pressure-Induced Renal Vasoconstriction Is Not Mediated by Increased Renal Sympathetic Nerve Activity and Is Abolished by High Salt Diet in Rats

Session Information

Category: Chronic Kidney Disease (Non-Dialysis)

  • 301 CKD: Risk Factors for Incidence and Progression

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
  • Cupples, William A., Simon Fraser University, Burnaby, British Columbia, Canada
  • Braam, Branko, University of Alberta, Edmonton, Alberta, Canada
Background

Combined cardiac/renal dysfunction may be perpetuated by elevated renal venous pressure (RVP). We demonstrated that renal nerves modulate the increase in renal vascular resistance (RVR) in response to mild but not severe RVP elevation. This suggests additional non-neural mechanisms. We hypothesized that mild RVP elevation would increase renal sympathetic nerve activity (RSNA) and that severe RVP elevation leads to vasoconstriction and diminished GFR via activation of the RAS. Objectives: (1) Measure renal sympathetic nerve activity in response to RVP elevation. (2) Evaluate RVP-induced modulation of renal hemodynamics following RAS suppression by high salt diet.

Methods

Blood pressure, RVP and RSNA were measured in anesthetized rats (300-400g, n=25). Separately, renal arterial blood flow (RBF) and GFR were assessed in rats (n=11) supplemented with 6% NaCl (2 weeks). In all rats, following baseline, RVP was increased to 10 or 20 mmHg by partial occlusion of the left renal vein for 120 min.

Results

RSNA was maintained in response to RVP 10 mmHg (frequency: 12.3±12.4%; amplitude: 0.06±0.2µV). RVP 20 mmHg induced a significant and sustained reduction in RSNA (-50.3±11.3%, p<0.05) and spike amplitude (-0.68±0.2µV, p<0.05). After high salt diet, RVP 10 or 20 mmHg did not elicit a change in RBF (RVP 10: -0.8±0.4ml/min; RVP 20: -1.0±0.4ml/min) and completely abolished the increase in RVR (RVP 10: -1.3±1.3mmHg.ml-1.min; RVP 20: -1.7±2.0mmHg.ml-1.min). High salt did not alter GFR response to RVP increase (RVP 10 GFR: -0.09±0.26ml/min; RVP 20 GFR: -1.11±0.28ml/min).

Conclusion

Mild RVP elevation sustains RSNA while severe RVP elevation supresses RSNA and reduces recruitment of nerve fibres. High salt-suppression of the RAS abolishes RVP-induced modulation of renal hemodynamics, indicating that the RAS, rather than RSNA mediates the renal response to acute RVP elevation.