Journal
JOURNAL OF PHYSIOLOGY-LONDON
Volume 596, Issue 7, Pages 1167-1179Publisher
WILEY
DOI: 10.1113/JP275545
Keywords
hypoxia; brain; blood flow; hypertension
Categories
Funding
- Brazilian National Council of Scientific and Technological Development (CNPq)
- Foundation for Research Support of Rio de Janeiro (FAPERJ)
- Coordination for the Improvement of Higher Education Personnel (CAPES)
- Brazilian Funding Agency for Studies and Projects (FINEP)
Ask authors/readers for more resources
Hypoxaemia evokes a repertoire of homeostatic adjustments that maintain oxygen supply to organs and tissues including the brain and skeletal muscles. Because hypertensive patients have impaired endothelial-dependent vasodilatation and an increased sympathetic response to arterial oxygen desaturation, we investigated whether hypertension impairs isocapnic hypoxia-induced cerebral and skeletal muscle hyperaemia to an extent that limits oxygen supply. In middle-aged hypertensive men, vertebral and femoral artery blood flow do not increase in response to isocapnic hypoxia, limiting brain and peripheral hyperaemia and oxygen supply. Increased chemoreflex-induced sympathetic activation impairs skeletal muscle perfusion and oxygen supply, whereas an attenuation of local vasodilatory signalling in the posterior cerebrovasculature reduced brain hyperperfusion of hypertensive middle-aged men in response to isocapnic hypoxia. The present study investigated whether hypertension impairs isocapnic hypoxia (IH)-induced cerebral and skeletal muscle hyperaemia to an extent that limits oxygen supply. Oxygen saturation (oxymetry), mean arterial pressure (photoplethysmography) and muscle sympathetic nerve activity (MSNA; microneugraphy), as well as femoral artery (FA), internal carotid artery and vertebral artery (VA) blood flow (BF; Doppler ultrasound), were quantified in nine normotensive (NT) (aged 4011years, systolic pressure 1197mmHg and diastolic pressure 736mmHg) and nine hypertensive men (HT) (aged 4412years, systolic pressure 15211mmHg and diastolic pressure 90 +/- 9mmHg) during 5min of normoxia (21% O-2) and IH (10% O-2). Total cerebral blood flow (tCBF), brain (CDO2) and leg (LDO2) oxygen delivery were estimated. IH provoked similar oxygen desaturation without changing mean arterial pressure. Internal carotid artery 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. Although increased chemoreflex-induced sympathetic activation may explain impaired peripheral perfusion, attenuated vasodilatory signalling in the posterior cerebrovasculature appears to be responsible for the small increase in tCBF when HT were exposed to IH.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available