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Hypertension. 1995;25:219-226

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(Hypertension. 1995;25:219-226.)
© 1995 American Heart Association, Inc.


Articles

Cellular Distribution of Angiotensin-Converting Enzyme After Myocardial Infarction

Mechthild Falkenhahn; Folker Franke; Rainer Maria Bohle; Yi-Chun Zhu; Harald Martin Stauss; Sebastian Bachmann; Sergei Danilov; Thomas Unger

From the Department of Pharmacology, University of Kiel (Germany) (M.F., Y.-C.Z., H.M.S., T.U.); the Department of Pathology, University of Giessen (Germany) (F.F., R.M.B.); the Department of Anatomy and Cell Biology, University of Heidelberg (Germany) (S.B.); and the National Cardiology Research Center, Moscow, Russia (S.D.).

Correspondence to Mechthild Falkenhahn, Department of Pharmacology, University of Kiel, Hospitalstr. 4, 24105 Kiel, FRG.

Abstract We studied the cellular distribution of angiotensin-converting enzyme (ACE) in the heart related to the cell types involved in left ventricular repair and remodeling before and after myocardial infarction by immunohistochemical techniques using monoclonal and polyclonal antibodies. In noninfarcted myocardium of both human and rat, ACE expression was confined to endothelial cells and subendocardial cell layers of the aortic valve. ACE was prominent in endothelia of small arteries and arterioles, whereas only half the coronary capillaries were immunoreactive and venous vessels were almost completely devoid of the enzyme. In a rat model of myocardial infarction, ACE distribution was determined 1, 3, and 7 days and 2, 3, and 6 weeks after coronary occlusion. Three and 7 days after infarction, endothelial cells of sprouting capillaries and macrophages in the marginal zone of necrosis revealed ACE expression. In both human and rat with the onset of fibrosis, intense staining of the enzyme was found in the marginal zone of the repair tissue. In situ hybridization for collagen type I in the rat revealed that zones with high collagen content had almost no ACE immunoreactivity. Vascular smooth muscle cells and cardiomyocytes revealed no ACE expression throughout the study. We conclude that endothelial cells are the principal source for the expression of ACE after myocardial infarction. The observed induction of ACE with the onset of fibrosis suggests a role of this enzyme that is related to tissue repair and remodeling.


Key Words: angiotensin-converting enzyme • heart • myocardial infarction • endothelium • macrophages




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