Physical (in)activity and endothelium-derived constricting factors: overlooked adaptations.
The inner surrounding of arterial vessels, the endothelium, is optimally located to detect changes in blood characteristics or blood flow that may result from changes in physical activity or from diseases. In response to physical stimuli, the endothelium varies its release of circulating vasoactive substances and serves as a source of local and systemic endothelium-derived dilator and vasoconstrictor factors. Endothelial dysfunction is one of the earliest markers of vascular abnormalities observed in cardiovascular disease and ageing. Exercise training is an efficient therapeutic strategy to improve endothelial function. Traditionally, studies on endothelial dysfunction and physical (in)activity-related effects on vascular adaptations are primarily focused on vasodilator substances (i.e. nitric oxide). One may suggest that augmentation of vasoconstrictor pathways (such as endothelin-1 and angiotensin II) contributes to the endothelial dysfunction observed after physical inactivity. Moreover, these pathways may also explain the exercise-induced beneficial cardiovascular adaptations. This review summarizes the current knowledge on the effects of physical (in)activity on several endothelium-derived vasoconstrictor substances.
Thijssen
D H J
DH
Department of Physiology, Radboud University Nijmegen Medical Centre, Geert Grooteplein-noord 21, 6525 EZ Nijmegen, the Netherlands. d.thijssen@fysiol.umcn.nl
Rongen
G A
GA
Smits
P
P
Hopman
M T E
MT
D000804:Angiotensin II / Q000502:physiology; D000818:Animals; D019332:Endothelin-1 / Q000502:physiology; D004730:Endothelium, Vascular / Q000503:physiopathology*; D006801:Humans; D009043:Motor Activity / Q000502:physiology*; D013928:Thromboxane A2 / Q000502:physiology; D014661:Vasoconstriction / Q000502:physiology*
D019332:Endothelin-1; D000804:Angiotensin II; D013928:Thromboxane A2