Proceedings of The Physiological Society

Europhysiology 2018 (London, UK) (2018) Proc Physiol Soc 41, PCA163

Poster Communications

Cardiovascular effects of capsaicin application on human skin at rest in temperate and warm conditions

P. G. Botonis1, P. G. Miliotis1, S. N. Kounalakis2, M. Koskolou1, N. D. Geladas1

1. School of Physical Education and Sports Sciences, National and Kapodistrian University of Athens, Greece, Daphne, Greece. 2. Faculty of Physical and Cultural Education, Evelpidon Hellenic Army Academy, Vari, Attica, Greece.


The heat-sensitive TRP vanilloid 1 (TRPV1) channels are stimulated at the heat-pain temperature of 43°C (1) or by capsaicin (2). It has been shown that capsaicin reduces the synthesis of prostaglandins, which stimulate the release of calcitonin gene-related peptide, a potent endogenous vasodilator (3), which, in turn, enhances Na+ excretion and nitric oxide release in endothelial cells (4). Thus, TRPV1 activation through capsaicin may have important potential for promoting cardiovascular health (5). To date, no study has elucidated whether TRPV1 stimulation has any effect on humans' blood pressure regulation. Therefore, we explored cardiovascular responses at rest in temperate (20°C) and warm (30°C) environment without and with application of capsaicin on the skin of human subjects. Ten healthy males were exposed, while seated, for 30 min to 20°C or 30°C on two occasions: without (NCA) and with (CA) skin application of capsaicin patches (12 x 18 cm), each one impregnated with of 4.0g capsaicin. In CA, one patch was applied on right pectoralis major muscle, another one on right trapezius and two more patches on the two vastus lateralis muscles. Mean arterial (MAP), systolic (SYS) and diastolic pressure (DIA), cardiac output (CO) and total peripheral resistance (TPR) were continuously measured via a photoplethysmometer (Finometer 2003, FMS, The Netherlands). Data were analyzed by 2-way ANOVA and the level of significance was set at p<0.05. Values are presented as mean±SD. MAP was lower (p≤0.01) when subjects were exposed at 30°C (98.6±7.7 mmHg) compared to 20°C (103.1±5.7 mmHg). Moreover, it was lower (p<0.01) in CA (98.7±7.9 mmHg) than in NCA condition (103.0±5.4 mmHg). Both SYS and DIA were lower (p≤0.01) in 30°C (131.0±9.8 and 79.0±7.7 mmHg, respectively) than in 20°C (140.3±9.2 and 81.5±4.6 mmHg, respectively) and in CA (133.3±12.4 and 78.1±6.8 mmHg, respectively) than in NCA condition (138.0±7.8 and 82.4±5.3 mmHg, respectively). No differences were detected in SYS and DIA among 20°C NCA, 20°C CA and 30°C NCA. Nonetheless, the mean values of SYS and DIA were lower (p<0.05) on average by 13.9 and 9.2 mmHg, respectively, in 30°C CA compared with the other three conditions. Regardless of capsaicin application, TPR was similar between 20°C and 30°C; it was lower (p=0.02), however, in CA than in NCA condition, with significant differences being evident only in 30°C. In addition, no differences were observed in CO among the experimental trials. At 30°C capsaicin induced arterial hypotension associated with vasodilation as indicated by the lower TPR. The absence of differences in blood pressure in CA at 20°C indicates a possible role of other heat-sensitive receptors on vascular relaxation. We conclude that the hypotensive effect of capsaicin is temperature-dependent.

Where applicable, experiments conform with Society ethical requirements