Effect of regular chilli consumption on endothelium-dependent and -independent vasodilation

Abstract

The active ingredient of chilli pepper, capsaicin, produces dose-dependent vasoconstriction in experimental animals (Griffiths et al., 1996). Although application of capsaicin locally to the skin induces vasodilation (Munce & Kenney, 2003), there is no information available on the effects of regular capsaicin consumption (in the form of chilli) on vascular function in humans. The aim of the present study was to determine the effects of chilli supplementation on endothelium-independent and endothelium-dependent vasodilatation. Fifteen non-smokers (M/F 7/8; aged 47.3 +/- 11.8 (+/- SD) years; weight 78.9 +/- 14.2 kg; body mass index 27.3 +/- 3.7 kg/m2) with no history of hypercholesteremia, diabetes mellitus or renal dysfunction consumed a chilli-free diet (normal diet with no chilli and minimal black pepper, ginger, etc) or chilli-supplemented diet (normal diet plus 30g/day Freshly chopped chilli(MasterFoods, Australia) for three weeks each. After three weeks on each diet, fasting peripheral and central (aortic) blood pressure, augmentation pressure (AP), augmentation index (AIx), AIx@HR75, heart rate and subendocardial viability ratio (Buckberg index) were determined using a sphygmomanometer and pulse wave analysis (SphygmoCor, AtCor, Australia) (Wilkinson et al, 2002). After adjusting for order and period of diet, mean (+/-SD) baseline AIx (27.97+/-2.70) and AIx@HR75 (19.40+/-2.00) were significantly lower (P<0.05) after the chilli diet compared to control diet (AIx, 23.97 +/- 2.73; AIx@HR75, 15.77 +/- 2.22). All parameters were then measured at regular intervals for 30 min after sublingual GTN (600 ug) and for 20 min after inhaled salbutamol (200 ug). Compared with the chilli-free period, there was no difference in the maximal change in any measured parameter or overall vasodilator response (AUC) in response to GTN or salbutamol after the chilli diet. These results suggest that regular chilli consumption reduces baseline vascular stiffness but has no significant effect on either endothelium-independent or -dependent vasodilatation.