The renin angiotensin
system (RAS) plays an all-encompassing role in cardiovascular regulation.
Indeed, the early notion defining its function as vasoconstrictive was expanded
to a much broader physiological spectrum, including sodium regulation and
structural cardiovascular changes. Moreover, many studies have shown the
synthesis and release of various components of the RAS in a number of organs.Further research revealed disparate RAS effects on vascular tone and sodiumexcretion. That is, RAS can induce vasoconstriction or vasodilatation,
natriuresis or sodium retention, hypertrophy or decreased proliferation, all
depending on a diversity of angiotensin peptides that can bind to different
receptors. The complexity of this system explains the multiplicity of its
effects.
Predictably,
inhibition of RAS at various levels potentially could yield multiple benefits.
Indeed, treatments with either angiotensin converting enzyme inhibitors (ACEi),
or angiotensin II receptor blockers (ARB’s) have shown important beneficial
effects, many of which are independent from hypertension control. Actually, RAS
inhibition is effective not only in treating essential hypertension, but also
in renovascular hypertension, heart failure, diabetic nephropathy, various
kidney diseases, (particularly when associated to heavy proteinuria),
atherosclerosis, acute coronary syndrome, vasculitis, ventricular hypertrophy,
atrial fibrillation, insulin resistance, multiple sclerosis and others.
Progression in most of these conditions is linked to RAS pathobiological
effects. Read more......................
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