Microvascular responses to aldosterone in hamster cheek pouch microcirculation.

The aim of the present study was to assess the in vivo effects of aldosterone topically applied on the hamster cheek pouch microcirculation under baseline conditions or during ischemia-reperfusion. Male Syrian hamsters were anesthetized, tracheotomized and intubated. They were studied under baseline conditions or submitted to ischemia-reperfusion. Cheek pouch microvessels were visualized by fluorescence microscopy. Microvascular parameters were determined by computerized methods. Under baseline conditions, aldosterone (0.2, 0.5, 2.4 μM/L/2 min) induced dose-dependent constriction of all arterioles within 2.0 ± 0.5 min of administration. Diameter reduction was in the same range in smaller arterioles: A3 ones constricted by 24 ± 3% of baseline (at the highest dose). Aldosterone applied prior to ischemia and at reperfusion caused arteriolar constriction, marked microvascular permeability (0.66 ± 0.03 Normalized Grey Level), reduction in perfused capillary (-70 ± 4% of baseline) and leukocyte adhesion. All changes were statistically significant compared with ischemic animals. Potassium canrenoate (mineralcorticoid receptor inhibitor) prior to aldosterone did not abolish the aldosterone-induced effects, while valsartan (angiotensin II AT1 receptor inhibitor) prior to aldosterone ameliorated microvascular ischemia-reperfusion injury. In conclusion, aldosterone determined dose-dependent arteriolar constriction likely by angiotensin II type-1 receptor activation (non-genomic mechanism) worsening the effects of ischemia-reperfusion on capillary perfusion, while protecting from free radical formation.