ACE2 activity is increased in monocyte-derived macrophages from prehypertensive subjects

Abstract

PreHTN subjects have higher ACE2-II activity compared with HTN subjects, suggesting a protective role for ACE2 in the early stage of HTN development, probably by accelerated degradation of the vasopressor AngII.

Recombinant Human Angiotensin-Converting Enzyme 2 as a New Renin-Angiotensin System Peptidase for Heart Failure Therapy

“…Consistent with a key role of ACE2 in post-MI remodeling, overexpression of ACE2 ameliorates left ventricular remodeling and dysfunction in a rat model of MI [36]. In the human population, genetic variability in the ace2 gene correlates with susceptibility to cardiovascular disease [37][38][39]. Single nucleotides polymorphisms of ACE2 are associated with variation in left ventricular mass, septal wall thickness, and ventricular hypertrophy [37]; coronary heart disease; and MI [38] and hypertension in patients with metabolic syndrome [40].…”

Contribution of the renin–angiotensin system in chronic foot-shock induced hypertension in rats

“…One of our interpretations is that the entire hypothalamus/cortex punches were harvested which could essentially impede the inference due to the heterogeneity of the ACE2 expression patterns in the different hypothalamic/cortex regions. It also may be due to a negative feedback mechanism in response to elevated blood pressure [16,38]; further study on the changes of Ang 1-7 in the tissues or plasma will provide more detailed evidence. Another explanation could be due to the different animal models applied in the experiments.…”

AT1receptor antagonism attenuates target organ effects of salt excess in SHRs without affecting pressure

“…Moreover, higher angiotensin-converting enzyme (ACE) and AT 1 binding have been recognized at the sites of cardiac injury, suggesting a contributory role of the local "de novo" angiotensin II synthesis (34,35). In addition, angiotensin II initiates and enhances inflammation and oxidative stress (17), and ACE has been detected in activated macrophages accounted for the initiation of the inflammatory response to tissue damage (15,19). Colocalization of inflammatory cells invading intramural coronary arteries with perivascular fibrosis and high ACE binding in an animal model of aldosterone/NaCl-induced cardiac injury support the reactive profibrotic role of locally produced angiotensin II (35).…”