What is the Origin of Counter-Regulatory Renin-Angiotensin System?

The discovery of this counter-regulatory axis emerged from advanced molecular research into the components of the classical RAS, which challenged the initial view of a singular, detrimental system. The subsequent identification of ACE2 and its product, Angiotensin-(1-7), revealed a critical, opposing force. This finding has significantly influenced the therapeutic approach to managing hypertension and heart failure.

What is the Mechanism of Counter-Regulatory Renin-Angiotensin System?

The core mechanism involves ACE2 converting Angiotensin II (Ang II), the primary vasoconstrictor of the classical RAS, into the heptapeptide Angiotensin-(1-7). Angiotensin-(1-7) then acts on the Mas receptor, triggering signaling cascades that promote vasodilation, reduce cellular proliferation, and exert an anti-inflammatory effect. This protective pathway serves as a vital physiological check against the detrimental effects of unchecked Ang II signaling.

Counter-Regulatory Renin-Angiotensin System ∞ Area

Counter-Regulatory Renin-Angiotensin System

Meaning

The Counter-Regulatory Renin-Angiotensin System (RAS) refers to a protective, homeostatic axis within the broader RAS, primarily mediated by the enzyme Angiotensin-Converting Enzyme 2 (ACE2) and the peptide Angiotensin-(1-7). This system functions to counterbalance the classical RAS pathway, which is pro-hypertensive, pro-fibrotic, and pro-inflammatory. It is a critical component of the body’s natural defense against cardiovascular and renal damage, promoting vasodilation and tissue repair.