TL;DRAbstract
The renin-angiotensin system (RAS) was originally described as a hemodynamic regulator that increases blood pressure acutely by vasoconstriction and chronically through aldosterone-mediated extracellular volume expansion (1). It is now clear that a tissue-based RAS exists, which is independently controlled from the circulation (2). Elevated tissue levels of components of the RAS including Ang II, the effector peptide of the RAS, have been demonstrated in numerous diseases independently of blood pressure elevation, such as Hypertension, atherosclerosis, myocardial infarction, cardiac failure, diabetes, and renal disease (2,3).
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The renin-angiotensin system (RAS) was originally described as a hemodynamic regulator that increases blood pressure acutely by vasoconstriction and chronically through aldosterone-mediated extracellular volume expansion (1). It is now clear that a tissue-based RAS exists, which is independently controlled from the circulation (2). Elevated tissue levels of components of the RAS including Ang II, the effector peptide of the RAS, have been demonstrated in numerous diseases independently of blood pressure elevation, such as Hypertension, atherosclerosis, myocardial infarction, cardiac failure, diabetes, and renal disease (2,3).
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