Atrial Natriuretic Peptide and Renal Dopaminergic System: A Positive Friendly Relationship?

Abstract

Sodium metabolism by the kidney is accomplished by an intricate interaction between signals from extrarenal and intrarenal sources and between antinatriuretic and natriuretic factors. Renal dopamine plays a central role in this interactive network. The natriuretic hormones, such as the atrial natriuretic peptide, mediate some of their effects by affecting the renal dopaminergic system. Renal dopaminergic tonus can be modulated at different steps of dopamine metabolism (synthesis, uptake, release, catabolism, and receptor sensitization) which can be regulated by the atrial natriuretic peptide. At tubular level, dopamine and atrial natriuretic peptide act together in a concerted manner to promote sodium excretion, especially through the overinhibition of Na+, K+-ATPase activity. In this way, different pathological scenarios where renal sodium excretion is dysregulated, as in nephrotic syndrome or hypertension, are associated with impaired action of renal dopamine and/or atrial natriuretic peptide, or as a result of impaired interaction between these two natriuretic systems. The aim of this review is to update and comment on the most recent evidences demonstrating how the renal dopaminergic system interacts with atrial natriuretic peptide to control renal physiology and blood pressure through different regulatory pathways.

Protective Renal Effects of Atrial Natriuretic Peptide: Where Are We Now?

“…ANP was discovered in 1981 by de Bold et al, (1981) as a 28-amino acid peptide that is synthesized and stored in atrial and ventricular myocytes and released in response to various stimuli, such as stretching of the cardiac wall, endothelin, diverse cytokines, or adrenergic agents ( Rukavina Mikusic et al, 2018b ). Subsequently, it has been described that the kidney has all the biosynthetic machinery to produce ANP, its receptors, and the catabolic enzymes to degrade it ( Wu et al, 2009 ; Choi et al, 2014 ). Given its actions in the kidney, it has been proposed that ANP could be involved in the pathogenesis of chronic kidney disease (CKD).…”

“…(2) At tubular level: ANP inhibits sodium reabsorption throughout the nephron ( Choi et al, 2014 ). In the proximal tubule, ANP inhibits different Na + transporters, as the Na + /H + exchanger, Na/Pi type IIa cotransporter, and the Na + , K + -ATPase, and also counteracts angiotensin-stimulated sodium reabsorption ( Theilig and Wu, 2015 ).…”

Alteration of Renal Natriuretic Systems Is Associated with the Development of Hypertension and Precedes the Presence of Renal Damage in a Model of Metabolic Syndrome

“…(11,12,22) Moreover, it has been shown that ANP increases the synthesis of renal dopamine by stimulating the activity of dopa decarboxylase. (31) In this insulin-resistance model, and as a result of low levels of plasma ANP, a reduction in both synthesis and uptake of dopamine by tubular cells would be expected as a consequence of reduced…”

Systemic Catecholaminergic Deficiency in Depressed Patients with and without Coronary Artery Disease

“…Peripheral dopamine plasma values are rarely reported in scientific literature, despite the fact that the dopaminergic system plays an important role in the cardiovascular system [ 44 ]. Dopamine might play a role in hypertension [ 55 ] and the role of a dopaminergic renal system in hypertension is discussed [ 56 ]. A recent study showed an inverse correlation between plasma dopamine and C-peptide concentrations in patients with diabetes, emphasizing modulating effects [ 57 ].…”