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Physical Overdistension Converts Ventricular Cardiomyocytes to Acquire Endocrine Property and Regulate Ventricular Atrial Natriuretic Peptide Production

Deborah Research Institute, Browns Mills, New Jersey

Michael D' Andrea

Deborah Research Institute, Browns Mills, New Jersey

Muralidharan Seethapathy

Deborah Research Institute, Browns Mills, New Jersey

Constance McDonnell

Deborah Research Institute, Browns Mills, New Jersey

Romuald Cichon

Deborah Research Institute, Browns Mills, New Jersey

Atrial natriuretic peptide (ANP) is present in adult atria but at very low concentrations in normal adult mamma lian ventricles. In the atria, the produc tion of ANP is regulated by physical distension of the atrial wall. The same phenomenon was investigated in the ventricles of rats and men. Cardiac tis sues from human ventricular aneurysm (n = 5), spontaneously hypertensive rats (n = 30), and rats that had overloaded left ventricles induced by surgery (n = 84) were studied with the methods of light microscopic immunocytochemis try, electron microscopic immunogold staining, and RNA-RNA tissue in situ hybridization. It was found that the levels of ANP gene expression, ANP im munoreactivity, and ANP-containing specific granules in the overburdened ventricles were elevated and their de grees of fluctuation were directly pro portional to the force of physical dis tension applied to the ventricular car diomyocytes. In rats, ANP mRNA and ANP immunoreactivity returned to the control level seven days after the ventri cular overload was surgically released. The changes of ANP and its mRNA in the ventricles were related more closely to the changes of intraventricular pres sure than to cardiocytic hypertrophy. In addition, ANP immunoreactivity was demonstrated in Purkinje cells and peri arteriolar cardiomyocytes in the ventri cles of normotensive rats. In conclusion, physical overstretch of the ventricle wall is likely to be the triggering factor affect ing ventricular cardiomyocytes to ac quire endocrine property, and also to regulate the production of ventricular ANP, thereby contributing to the con trol of the blood volume and the blood pressure.

Angiology, Vol. 42, No. 3, 173-186 (1991)
DOI: 10.1177/000331979104200301


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