Mechanisms for the release of atrial natriuretic peptide

Abstract

In assessing the role that atrial natriuretic peptide (ANP) might have in the homeostasis of fluid volume and blood pressure, it is important to define the physiological and pathophysiological conditions that determine its release into the circulation. There is substantial evidence that ANP is released through atrial distension under a variety of conditions. There are also some indications that ANP may be released through humoral factors, although it is not clear whether this is a result of direct action on the myocytes or simply a result of ensuing haemodynamic changes. There is no evidence to suggest that ANP can be released through stimulation of efferent fibres innervating the atria, but it may be released as a result of changes in myocardial work and oxygen consumption. Plasma levels of ANP are elevated in several disease states and that release appears to be a result of the haemodynamic disturbances in those conditions.

Release of atrial natriuretic peptide during pulmonary arteryclamping in man

“…However, low-dose infusions of ANP over longer periods (hours to days), producing p-ANP concentrations within the Introduction Atrial peptides, a family of cardiac hormones with cardiovascular and renal effects (de Bold et al, 1981;Goetz, 1988), are produced in and released from the heart. Stretch of the atrial wall seems to be the most important releasing factor (for review, see Rankin, 1987), which is reflected by a rise in plasma atrial natriuretic peptide (p-ANP) during mitral obstruction (Ledsome et al, 1985) or volume loading (Lang et al, 1985). The role of ANP as a physiologically important hormone has been questioned, especially as initial studies showed that only supraphysiological concentrations gave any renal response in different experimental models (Goetz, 1990).…”

Proceedings of the Physiological Society, 9‐10 January 1992, Manchester Meeting: Communications

“…It is well established that one stimulus for the secretion of atrial natriuretic factor (ANF) is atrial stretch. There is some evidence suggesting circulating hormones may also increase the secretion (Rankin, 1987), and we have shown (Speake et al 1991) a stimulation of secretion with adrenaline and an inhibition with acetylcholine suggesting a possible role for the autonomic nervous system. Adrenaline has also been shown to increase both rate and force of contraction.…”

The RAF Kinase Inhibitor Protein (RKIP): Good as Tumour Suppressor, Bad for the Heart

“…Taken together, RKIP exerts cardiotoxic effects by multiple pathways (i) as a tumour metastasis suppressor and inhibitor of the RAF1-MAPK axis and (ii) as a GRK2 inhibitor (Figure 7). cAMP signalling and upregulation of natriuretic peptides NPPA and NPPB [162,163]. In support of this statement, Tg-RKIP hearts with symptoms of heart failure showed upregulation of Grk2, which reflects sensitised β-adrenoceptor-stimulated cAMP signalling [142].…”

“…By sensitisation of the heart failure-promoting Gq/11-coupled AGTR1, RKIP enhances myocardial fibrosis and cardiac hypertrophy [ 10 , 21 , 22 , 23 ]. By sensitisation of cardiac Gs-coupled β-adrenoceptors, RKIP could promote detrimental Gs-stimulated cAMP signalling and upregulation of natriuretic peptides NPPA and NPPB [ 162 , 163 ]. In support of this statement, Tg-RKIP hearts with symptoms of heart failure showed upregulation of Grk2 , which reflects sensitised β-adrenoceptor-stimulated cAMP signalling [ 142 ].…”