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Fig. 2 | Respiratory Research

Fig. 2

From: Autonomic nervous system involvement in pulmonary arterial hypertension

Fig. 2

Renin-angiontensin-aldosterone system (RAAS) activation in PAH. Renin cleaves angiotensinogen to angiotensin I, which is further processed by the angiotensin-converting enzyme (ACE) to the biologically active peptide angiotensin II and binds to angiotensin receptors AT1 and AT2. Angiotensin I and II may also undergoe further processing by ACE2 to yield angiotensin (1–7), which activates the Mas receptor. On the other hand, aldosterone activates the mineralocorticoid receptors. Both AT1 and mineralocorticoid receptor activation lead to pathological signaling in PAH, and targeting these pathways using receptor antagonists or ACE inhibitors improves PAH. On the other hand, AT2 and Mas signaling are protective, and promoting these signaling cascades using AT2 agonists or ACE2 activators improves autonomic nervous system imbalance seen in PAH

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