Insufficient secretion of atrial natriuretic peptide at acute phase of myocardial infarction

Abstract

To investigate the secretion of the plasma levels of atrial natriuretic peptide (ANP) in patients with acute myocardial infarction (AMI), we evaluated the relationship between plasma levels of ANP and pulmonary capillary wedge pressure (PCWP) in 45 consecutive patients during the acute phase of AMI ( approximately 12 h after the attack) (group 1) and compared data with those obtained after 1 mo (group 2). In both groups 1 and 2, plasma ANP levels significantly correlated with PCWP. The slope of the linear regression line between the PCWP and ANP in group 1 was significantly lower, by about one-third, than that in group 2. In addition, we examined changes in ANP levels and left ventricular end-diastolic pressure (LVEDP) over 180 min after AMI induced by injection of microspheres into the left coronary arteries of three dogs. The LVEDP and ANP levels 30 min after AMI were significantly higher than those before; however, despite the persistent high LVEDP during the 180 min after AMI, ANP levels decreased gradually and significantly to 63% of the peak level at 150 min. These findings suggest that the secretion of ANP during the acute phase of myocardial infarction may be insufficient relative to the chronic phase.

Evaluation of NT‐Pro BNP and CT‐ANP as Markers of Concentric Hypertrophy in Dogs with a Model of Compensated Aortic Stenosis

“…Regulation of the synthesis and release of ANP and BNP has been reported to differ 32–34 . Plasma ANP is increased immediately but plasma BNP is slowly increased as a consequence of hemodynamic changes.…”

“…Plasma ANP is increased immediately but plasma BNP is slowly increased as a consequence of hemodynamic changes. Maeda et al 32 showed that LVEDP and ANP concentrations were significantly increased from baseline 30 minutes after acute myocardial infarction. However, despite persistently high LVEDP after 180 minutes, ANP concentrations decreased significantly to 63% of the peak level.…”

Comparison of N-terminal pro-atrial natriuretic peptide and three cardiac biomarkers for discriminatory ability of clinical stage in dogs with myxomatous mitral valve disease

“…In dogs with MMVD, CBs, other than plasma ANP and NT-proANP concentrations, have clinical utility include plasma N-terminal pro-brain natriuretic peptide (NT-proBNP) and cardiac troponin I (cTnI) concentrations [ 14 , 16 , 33 , 34 ]. NT-proBNP is released into the blood circulation primarily in response to ventricular myocyte stretch, and cTnI is released into the blood with cardiomyocyte injury.…”

AT1 receptor blockade increases cardiac bradykinin via neutral endopeptidase after induction of myocardial infarction in rats

“…Although the role of cardiac NEP in the repair of infarcted myocardium is not clear, the natriuretic pep‐tide and/or kinin system may be involved through this up‐regulation, since NEP is responsible for the breakdown of ANP/BNP and BK. Thus, the increased NEP activity in the infarcted area would reduce not only ANP concentrations (7) but also BK levels. However, we found an increase of myocardial BK levels in infracted areas of untreated rats, indicating that kinin concentrations in the myocardium are partially determined by factors other than kinin‐degrading enzymes.…”

“…BK was quantitated by a specific RIA, as described previously (6). The antiserum displayed a 36% cross-reactivity to T-kinin and had no affinity to smaller kinin fragments such as [1][2][3][4][5][6][7][8]…”