René van der Bel

| Chapter 5 | 86 Abstract There is ample evidence that systemic sympathetic neural activity contributes to the progres- sion of chronic kidney disease, possibly via limiting renal blood flow and thereby inducing renal hypoxia. Up to now there are no direct observations of this mechanism in humans. We studied the effects of systemic sympathetic activation by Lower Body Negative Pressure (LBNP) on renal blood flow (RBF) and renal oxygenation in healthy humans. Eight healthy volunteers (age 19-31 years) were subjected to progressive LBNP. Brachial artery blood pressure was monitored intermittently. RBF was measured by phase contrast MRI in the proximal renal artery. Renal vascular resistance was MAP divided by RBF. Renal oxygenation (R2*) was measured for the cortex and medulla by Blood Oxygen Level Depen- dent (BOLD) MRI, using a mono-exponential fit. During -30 mmHg LBNP, pulse pressure decreased from 50±10 to 43±7 mmHg; MAP did not change. RBF decreased from 1152 ± 80 to 1038 ± 83 mL/min to 950 ± 67 mL/min at -30 mmHg LBNP (p = 0.013). Heart rate and renal vascular resistance increased by 38±15% and 23±8% (p=0.04), respectively There was no change in cortical or medullar R2* (20.3 ± 1.2 s -1 vs 19.8 ± 0.43 s -1 ; 28.6 ± 1.1 s -1 vs 28.0 ± 1.3 s -1 ). Our results indicate that sympathetic activation decreases kidney perfusion without a paral- lel reduction of oxygenation in healthy humans.