Atrial Natriuretic Peptide31–67: A Novel Therapeutic Factor for Cardiovascular Diseases

Abstract

The characterization of the cardiac hormone atrial natriuretic peptide (ANP99–126), synthesized and secreted predominantly by atrial myocytes under stimulation by mechanical stretch, has established the heart as an endocrine organ with potent natriuretic, diuretic, and vasodilating actions. Three additional distinct polypeptides resulting from proteolytic cleavage of proANP have been identified in the circulation in humans. The mid-sequence proANP fragment 31–67 (also known as proANP31–67) has unique potent and prolonged diuretic and natriuretic properties. In this review, we report the main effects of this circulating hormone in different tissues and organs, and its mechanisms of actions. We further highlight recent evidence on the cardiorenal protective actions of chronic supplementation of synthetic proANP31–67 in preclinical models of cardiorenal disease. Finally, we evaluate the use of proANP31–67 as a new therapeutic strategy to repair end-organ damage secondary to hypertension, diabetes mellitus, renal diseases, obesity, heart failure, and other morbidities that can lead to impaired cardiac function and structure.

Epigenetic and Genetic Mechanisms Underlying Cardiovascular Diseases and Neurodevelopmental Disorders

“…Benign familial infantile epilepsy is an autosomal dominant epilepsy that was first reported by Vigevano et al (11) and was named BFIE in 2010 by the International League Against Epilepsy (ILAE) 10.3389/fneur.2023.1135044 Frontiers in Neurology 03 frontiersin.org (12). The main clinical criteria for diagnosis (13) include ( 1) first onset at 3-12 months old, (2) family history of benign infantile epilepsy, (3) normal psychomotor development before and after onset, (4) focal seizures, alone or followed by generalized seizures, with ≥2 seizures within 24 h, mostly cluster seizures, usually without persistent status epilepticus, (5) normal EEG background during interictal periods with Rolandic epilepsy, (6) no abnormalities in cranial imaging, (7) exclusion of convulsions due to metabolic disorders such as hypocalcemia and hypoglycemia, and ( 8) self-limiting seizures or seizures that respond well to antiepileptic drugs, with resolution before the age of 2 years old (14,15).…”

“…ANP is encoded by the NPPA gene (10) located on chromosome 1 in the human genome and is primarily expressed by atrial myocytes. ANP derives from its precursors pre-pro-ANP and pro-ANP (11).…”

Exploring the Complex Relationship between Diabetes and Cardiovascular Complications: Understanding Diabetic Cardiomyopathy and Promising Therapies

“…Activation of RAAS, vasopressin, and the sympathetic nervous system leads to increased ventricular preload, afterload, and elevated wall stress, thereby causing the production of pre-pro BNP, which is further cleaved to BNP and N-terminal pro-BNP (NT-pro-BNP), which is a physiologically inactive form. In contrast, atrial stretching ultimately leads to the production of pre-pro-atrial or A-type natriuretic peptide and further ANP, which has a similar biological characteristic to BNP in promoting natriuresis and vasodilation [ 120 , 121 , 122 ]. Neprilysin plays a key role in the degradation of these peptides and hence complicates the underlying mechanism in cardiovascular events.…”

FTIR Analysis of Renal Tissue for the Assessment of Hypertensive Organ Damage and proANP31–67 Treatment

“…To achieve this aim, we used Dahl/salt-sensitive (DSS) rats and monitored the kidney damage at six weeks of salt-induced hypertension. In the present work, FTIR analysis was also applied to investigate the effect of proANP 31–67 , a linear fragment of pro-atrial natriuretic peptide [ 17 ]. This drug was recently developed to enhance renal function [ 18 ]; however, its effects on renal tissue have not been fully characterized.…”