Hypertension is characterized by a pro-inflammatory status, including redox imbalance
and increased levels of pro-inflammatory cytokines, which may be exacerbated after
heat exposure. However, the effects of heat exposure, specifically in individuals
with inflammatory chronic diseases such as hypertension, are complex and not well
understood. This study compared the effects of heat exposure on plasma cytokine
levels and redox status parameters in 8 hypertensive (H) and 8 normotensive (N)
subjects (age: 46.5±1.3 and 45.6±1.4 years old, body mass index: 25.8±0.8 and
25.6±0.6 kg/m2, mean arterial pressure: 98.0±2.8 and 86.0±2.3 mmHg,
respectively). They remained at rest in a sitting position for 10 min in a
thermoneutral environment (22°C) followed by 30 min in a heated environmental chamber
(38°C and 60% relative humidity). Blood samples were collected before and after heat
exposure. Plasma cytokine levels were measured using sandwich ELISA kits. Plasma
redox status was determined by thiobarbituric acid reactive substances (TBARS) levels
and ferric reducing ability of plasma (FRAP). Hypertensive subjects showed higher
plasma levels of IL-10 at baseline (P<0.05), although levels of this cytokine were
similar between groups after heat exposure. Moreover, after heat exposure,
hypertensive individuals showed higher plasma levels of soluble TNF receptor (sTNFR1)
and lower TBARS (P<0.01) and FRAP (P<0.05) levels. Controlled hypertensive
subjects, who use angiotensin-converting-enzyme inhibitor (ACE inhibitors), present
an anti-inflammatory status and balanced redox status. Nevertheless, exposure to a
heat stress condition seems to cause an imbalance in the redox status and an
unregulated inflammatory response.