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Article type: Research Article
Authors: Lapi, Dominga | Emdin, Michele | Mastantuono, Teresa | Sapio, Daniela | Santillo, Mariarosaria | Colantuoni, Antonio
Affiliations: Department of Neuroscience, “Federico II” University Medical School, Naples, Italy | CNR Institute of Clinical Physiology, Pisa, Italy | Department of Neuroscience, Section of Pharmacology, “Federico II” University Medical School of Naples, Naples, Italy
Note: [] Corresponding author: Dominga Lapi, PhD, Department of Neuroscience, “Federico II” University Medical School, Via S. Pansini, 5, Naples 80131, Italy. Tel.: +39 081 7463212; Fax: +39 081 5453045; E-mail: [email protected]
Abstract: 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.
Keywords: Hamster cheek pouch microcirculation, ischemia-reperfusion, aldosterone, mineral corticoid receptor, angiotensin II AT\(_{\rm{1}}\) receptor
DOI: 10.3233/CH-2012-1552
Journal: Clinical Hemorheology and Microcirculation, vol. 53, no. 4, pp. 303-315, 2013
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