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Submitted on January 17, 2006
Accepted on April 3, 2006
Chair of Internal Medicine and Chair of General Surgery, Department of Medical and Surgical Sciences; Chair of Human Anatomy, Department of Biomedical Sciences and Biotechnology, University of Brescia, Italy
* To whom correspondence should be addressed. E-mail: rizzoni{at}med.unibs.it.
Context and Objective It has been previously demonstrated that aldosterone may possess a strong profibrotic action in vitro and in animal models of genetic or experimental hypertension. Our aim was to evaluate whether such a profibrotic action is present also in the human microcirculation.
Design and Patients We investigated 13 patients with primary aldosteronism, 7 patients with essential hypertension and 10 normotensive controls. All subjects were submitted to a biopsy of gluteal sc fat tissue. Small resistance arteries were dissected and mounted on an isometric myograph and the tunica media to internal lumen ratio was measured.
Main outcome measures The total collagen content within the tunica media was detected (Sirius red staining and image analysis) and collagen subtypes were evaluated using polarized light microscopy; under this condition thicker type I collagen fibers appear orange or red, while thinner type III collagen fibers are yellow or green.
Results Tunica media to internal lumen ratio was significantly increased in primary aldosteronism and in essential hypertension compared with normotensive controls. Clinic blood pressure values were similar in primary aldosteronism and in essential hypertension and greater than in normotensive controls. Normotensive controls had less total and type III collagen (3.23 ± 0.58% and 1.60 ± 0.22%, respectively) in respect with the two hypertensive groups (P < 0.001). Total collagen and type III vascular collagen were significantly greater in primary aldosteronism (total collagen: 8.17 ± 1.38%, type III collagen:6.06 ± 0.74%, P < 0.05) than in essential hypertension (total collagen: 6.84 ± 1.15%, type III collagen: 5.25 ± 0.80%).
Conclusions Our results indicate that in small resistance arteries of patients with primary aldosteronism a pronounced fibrosis may be detected, even more evident that in blood-pressure matched patients with essential hypertension.
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