A Cross-Talk between the Renin-Angiotensin and Adrenergic Systems in Cardiovascular Health and Disease

Abstract

It is well accepted that a number of cardiovascular (CV) and renal diseases are characterized by the long-term activation of both the renin-angiotensin system (RAS) and the sympathetic nervous system (SNS), which also contribute to the pathophysiology of structural and functional CV abnormalities as well as to the final clinical outcome. Moreover, there is a growing body of conclusive evidence that these systems do not operate independently, but interact at different levels throughout the CV
system. The mediation of renin release from juxtaglomerular epithelioid (JGE) cells in kidney by SNS is well established and accepted. On the other hand, in recent years it became evident that RAS, by its main effect or angiotensin II (Ang II), induces SNS activity in various organs and tissues. Thus, there is a growing effort to clarify pathophysiological mechanisms of interaction and a more evident mutual potentiation of these two systems in different pathological states. Since it became evident that a high salt (HS) intake, which is a major risk factor for hypertension development, has a deleterious impact on vascular and endothelial functions (even in the absence of blood pressure changes), it became necessary to investigate and clarify the effect of HS loading on major regulating systems—RAS and
SNS—precisely in healthy individuals. The present review aimed to summarize the interactions between the RAS and SNS in health and diseases (e.g. cardiovascular, renal), with a special focus on these two systems’ interaction during HS intake in a healthy normotensive population.