Angiotensin-converting enzyme inhibition stimulates fracture healing and periosteal callus formation in mice
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چکیده
INTRODUCTION: The renin angiotensin system (RAS) is classically known as circulating endocrine system, regulating blood pressure and electrolyte homeostasis. The main effector peptide in this system is Angiotensin II (Ang II), which is hydrolized from angiotensin I (Ang I) by the angiotensin converting enzyme (ACE), a key molecule in this system. Angiotensin I, however, is cleaved from angiotensinogen by renin. Ang II exerts its biological effects through binding with different specific angiotensin receptors, mainly the angiotensin type 1 and 2 receptors (AT1-receptor and AT2-receptor). The ACE furthermore interferes with the kallikrein-kinin system by degradation of bradykinin, which is responsible for prostaglandine (PG) and nitric oxide (NO) production through binding with specific receptors (B1 and B2).
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