Reduced arterial vasodilation in response to hypoxia impairs cerebral and peripheral oxygen delivery in hypertensive men

Abstract

This study investigated whether hypertension impairs isocapnic hypoxia (IH)-induced cerebral and skeletal muscle hyperemia to an extent that limits oxygen supply. Oxygen saturation (Oxymetry), mean arterial pressure (MAP, photoplethysmography), muscle sympathetic nerve activity (MSNA, microneugraphy), and femoral (FA), internal carotid (ICA) and vertebral (VA) artery blood flow (BF, Doppler ultrasound) were quantified in 9 normotensive (NT, 40 ± 11 yrs., systolic (SP) 119 ± 7 mmHg and diastolic pressure (DP) 73 ± 6 mmHg) and 9 hypertensive men (HT, 44 ± 12 yrs., SP 152 ± 11 mmHg and DP 90 ± 9 mmHg) during 5 min of normoxia (NX – 21% O₂) and IH (10% O₂). Total cerebral blood flow (tCBF), brain (CDO₂) and leg (LDO₂) oxygen delivery were estimated. IH provoked similar oxygen desaturation without changing MAP. ICA perfusion increased in both groups during IH. However, VA and FA BF only increased in NT. Thus, IH-induced increase in tCBF was smaller in HT. CDO₂ only increased in NT and LDO₂ decreased in HT. Furthermore, IH evoked a greater increase in HT MSNA. Changes in MSNA were inversely related to FA BF, LDO₂ and end-tidal oxygen tension. In conclusion, hypertension disturbs regional and total cerebrovascular and peripheral responses to IH and consequently limits oxygen supply to the brain and skeletal muscle. While increased chemoreflex-induced sympathetic activation may explain impaired peripheral perfusion, attenuated vasodilatory signalling in the posterior cerebrovasculature seems responsible for the small increase in tCBF when HT were exposed to IH.

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