An Influence of Angiotensin II on Heat Loss Responses in Humans during Intermittent Exercise in the Heat: a Role for Oxidative Stress

Abstract

Angiotensin II (Ang II) has been implicated in the pathophysiology of cardiovascular disease through several mechanisms, including evoking elevations in oxidative stress. We tested the hypothesis that increases in oxidative stress induced by Ang II impair the local heat loss responses of cutaneous vasodilation and sweating. Eleven young (24 ± 4 years) healthy adults (7 males, 4 females) performed two 30‐min cycling bouts at a fixed rate of metabolic heat production (400 W; equivalent to ~47 %VO2max) in the heat (35 ºC). Exercise was separated by 20 and 40 min of recovery, respectively.Sweat rate (ventilated capsule) and cutaneous vascular conductance (CVC, laser‐Doppler perfusion units/mean arterial pressure) were evaluated at four skin sites receiving either: 1) lactated Ringer (Control), 2) 10 μM Ang II, 3) 10 mM ascorbate (an antioxidant), or 4) a combination of 10 μM Ang II + 10 mM ascorbate via microdialysis. Compared to Control, Ang II reduced both CVC and sweating at baseline rest and during each recovery (all P < 0.05). When ascorbate was co‐infused with Ang II, the effect of Ang II on CVC at baseline rest and during each recovery remained intact (all P < 0.05), whereas its effect on sweating was abolished (all P > 0.05). No differences in CVC or sweating between the four treatment sites were observed during either exercise bouts (all P > 0.05). Thus, we show that at rest and during postexercise recovery in the heat, Ang II impairs cutaneous vasodilation independent of oxidative stress, while it impairs sweating through increases in oxidative stress. Support: Natural Sciences and Engineering Research Council of Canada (RGPIN‐06313‐2014).