Abstract
Besides pumping, the heart participates in hydro-sodium homeostasis and systemic blood pressure regulation through its endocrine function mainly represented by the large family of natriuretic peptides (NPs), including essentially atrial natriuretic (ANP) and brain natriuretic peptides (BNP). Under normal conditions, these peptides are synthesized in response to atrial cardiomyocyte stretch, increase natriuresis, diuresis, and vascular permeability through binding of the second intracellular messenger’s guanosine 3′,5′-cyclic monophosphate (cGMP) to specific receptors. During heart failure (HF), the beneficial effects of the enhanced cardiac hormones secretion are reduced, in connection with renal resistance to NP. In addition, there is a BNP paradox characterized by a physiological inefficiency of the BNP forms assayed by current methods. In this context, it appears interesting to improve the efficiency of the cardiac natriuretic system by inhibiting cyclic nucleotide phosphodiesterases, responsible for the degradation of cGMP. Recent data support such a therapeutic approach which can improve the quality of life and the prognosis of patients with HF.
Highlights
Over the past decades, much work supported the hypothesis that the heart has a mechanical and an endocrine function
Within the natriuretic peptides (NPs) family, we describe the biochemical, physiological, and pathophysiological characteristics of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP)
Hypoxia-sensitive elements were found in the BNP and ANP gene promoter sequences [75,76]. In relation to this process, Stockmann et al [77] studied the effects of oxygenation on enlarged cardiac ventricles and showed in rats that, when normoxia conditions are restored, the ANP content decreases towards control rat levels despite persistent hypertrophy
Summary
Much work supported the hypothesis that the heart has a mechanical and an endocrine function. The existence of hormonal systems in the heart tissue (i.e., the biochemical components necessary for hormone synthesis) provides the heart with the ability of participating in cardiovascular homeostasis and metabolism in addition to its pumping function. These cardiac hormones may affect remote tissues (endocrine function of the heart) and/or have local effects (paracrine and autocrine actions) [1,2], which may influence the action of cyclic nucleotide phosphodiesterases (PDEs). We will review both natriuretic peptides physiology and pathology, focusing on their roles in cardiac failure and on the implications of the PDEs family, which might open new therapeutic approaches
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