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Abstract
Circulating renin-angiotensin-aldosterone system (RAAS) activation is a classic endocrine response that plays an important role in cardiovascular homeostasis during physiologic and pathologic states. There is now accumulating evidence that locally-generated angiotensin II (AngII) has important autocrine and paracrine functions in a variety of organs [1, 2] including a role in regulating tissue structure. Most components of the RAAS have been found in the vasculature [3, 4]. A role for local AngII in tissue repair, including the heart, has recently attracted attention [5, 6]. Following myocardial infarction (MI), a wound healing response occurs in infarcted and noninfarcted tissue of the rat heart. Healing results in an extensive structural remodeling of the heart expressed as fibrous tissue accumulation at and remote to the site of MI. Chemical mediators of exudative and inflammatory phases of healing include various substances, such as bradykinin (BK) and prostaglandins (PG) [7], and more recently discovered regulatory peptides [8, 9] generated within tissue at the site of repair. Mediators of the fibroplastic and fibrogenic phases of healing, likewise produced at the site of repair, are under investigation. In this connection, a role for locally-produced peptides (eg., AngII) in regulating healing with fibroblast growth and collagen turnover has been considered [10, 11]. Increasing evidence indicates local AngII production plays an important role in tissue repair [12, 13]. Herein we review recent studies of wound healing in the rat heart and locally-generated AngII.
Published Version
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