René van der Bel

| Chapter 3 | 40 Abstract Renal hypoxia is thought to be an important pathophysiological factor in the progression of chronic kidney disease (CKD) and the associated hypertension. In a previous study among CKD patients, supplementation with 100% oxygen reduced sympathetic nerve activity (SNA) and lowered blood pressure (BP). We aimed to assess the underlying haemodynamic modu- lation and hypothesized a decreased systemic vascular resistance (SVR). To that end, 19 CKD patients were studied during 15-minute intervals of increasing partial oxygen pressure (ppO 2 ) from room air (0.21 ATA) to 1.0 ATA and further up to 2.4 ATA, while continuously measuring finger arterial blood pressure (Finapres). Off-line, we derived in- dexes of SVR, cardiac output (CO) and baroreflex sensitivity from the continuous BP record- ings (Modelflow). During oxygen supplementation, systolic and diastolic BP both increased dose-dependently from 128±24 and 72±19 mmHg respectively at baseline to 141±23 (p<0.001) and 80±21 mmHg (p<0.001) at 1.0ATA oxygen. Comparing baseline and 1.0 ATA oxygen, SVR increased from 1440±546 to 1745±710dyn·s/cm 5 (p=0.009), heart rate decreased from 60±8 to 58±6 bpm (p<0.001) and CO from 5.0±1.3 to 4.6±1.1 L/min (p=0.02). Baroreflex sensitivity re- mained unchanged (13±13 to 15±12 ms/mmHg). These blood pressure effects were absent in a negative control group of eight young healthy subjects. We conclude that oxygen supplementation in CKD patients causes a non-baroreflex medi- ated increased in SVR and blood pressure.