Natriuretic peptides and cardio-renal disease Massimo Volpe  International Journal of Cardiology  Volume 176, Issue 3, Pages 630-639 (October 2014) DOI: 10.1016/j.ijcard.2014.08.032 Copyright © 2014 The Author Terms and Conditions

Fig. 1 Schematic diagram to show how the NP system, the RAAS and the SNS interact in order to maintain cardio-renal homeostasis, and how the effects of the NP system and the RAAS on key organs are generally counter-regulatory. ACE=angiotensin converting enzyme; Ang=angiotensin; ANP=atrial natriuretic peptide; BNP=B-type natriuretic peptide; BP=blood pressure; NP=natriuretic peptide; RAAS=renin–angiotensin–aldosterone system; SNS=sympathetic nervous system. International Journal of Cardiology 2014 176, 630-639DOI: (10.1016/j.ijcard.2014.08.032) Copyright © 2014 The Author Terms and Conditions

Fig. 2 Schematic representation to show the mode of action of an ARNI. NPs are degraded to inactive fragments by the enzyme NEP. Inhibition of NEP by an ARNI enhances NP levels, leading to biological effects that may have the potential to benefit CV health. However, Ang II is also a substrate for NEP, so NEP inhibition may lead to increased Ang II levels. Through blockade of the AT1 receptor, an ARNI simultaneously suppresses the RAAS to counter the detrimental effects of elevated Ang II. Ang II=angiotensin II; ARNI=angiotensin receptor neprilysin inhibitor; AT1=angiotensin type 1 receptor; CV=cardiovascular; NEP=neprilysin; NP=natriuretic peptide; NPR =natriuretic peptide receptor; RAAS = renin–angiotensin–aldosterone system. International Journal of Cardiology 2014 176, 630-639DOI: (10.1016/j.ijcard.2014.08.032) Copyright © 2014 The Author Terms and Conditions