Blood Pressure Increase during Oxygen Supplementation in Chronic Kidney Disease Patients Is Mediated by Vasoconstriction Independent of Baroreflex Function

• Published in: Frontiers in physiology 2017-03, Vol.8, p.186-186
• Main Authors: van der Bel, René, Çalişkan, Müşerref, van Hulst, Robert A, van Lieshout, Johannes J, Stroes, Erik S G, Krediet, C T Paul
• Format: Article
• Language: English
• Subjects: Physiology
• ISSN: 1664-042X; 1664-042X
• DOI: 10.3389/fphys.2017.00186

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 modulation and hypothesized a decreased systemic vascular resistance (SVR). To that end, 19 CKD patients were studied during 15-min intervals of increasing partial oxygen pressure (ppO ) 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 indexes of SVR, cardiac output (CO) and baroreflex sensitivity from the continuous BP recordings (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 ( < 0.001) and 80 ± 21 mmHg ( < 0.001) at 1.0 ATA oxygen. Comparing baseline and 1.0 ATA oxygen, SVR increased from 1440 ± 546 to 1745 ± 710 dyn·s/cm ( = 0.009), heart rate decreased from 60 ± 8 to 58 ± 6 bpm ( < 0.001) and CO from 5.0 ± 1.3 to 4.6 ± 1.1 L/min ( = 0.02). Baroreflex sensitivity remained 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 mediated increased in SVR and blood pressure.