The relationships of
cortisol with elevated blood pressure and
insulin resistance are likely to be the result of a complex interplay of different mechanisms. We hypothesize that
cortisol is associated with impaired microvascular function and that this contributes to
cortisol-associated
high blood pressure and
insulin resistance. We examined 24 h urinary free
cortisol excretion in 56 healthy adults (26 women). Blood pressure was assessed by 24 h ambulatory measurements.
Insulin sensitivity was determined using the hyperinsulinaemic euglycaemic clamp technique. Skin capillary recruitment after
arterial occlusion was visualized with videomicroscopy and endothelium-(in)dependent vasodilation was evaluated with iontophoresis of
acetylcholine and
sodium nitroprusside combined with
laser Doppler fluxmetry. Men were characterized by higher urinary
cortisol excretion [median (interquartile range), 162 (130-194) compared with 118 (99-156) nmol/24 h, P<0.05]. In women, but not in men, urinary
cortisol excretion was associated with impaired capillary recruitment (r=-0.66, P<0.001), higher systolic blood pressure (r=0.64, P<0.001) and lower
insulin sensitivity (r=-0.43, P<0.05). Urinary
cortisol excretion was not associated with endothelium-(in)dependent vasodilation in men or women. Regression analysis demonstrated that capillary recruitment statistically explained 37% of the association between urinary
cortisol and blood pressure in women. Capillary recruitment did not explain part of the association between urinary
cortisol and
insulin sensitivity. In conclusion, urinary
cortisol excretion is inversely associated with capillary recruitment in women, but not in men, and capillary recruitment explains part of the
cortisol-blood pressure relationship. These data suggest that, in women, impairment of capillary function mediates some of the adverse effects of
cortisol and thus may provide a target to prevent such adverse effects.