Cellular mechanisms of growth in cardiovascular tissue.
Left ventricular hypertrophy is a complex cellular response to a variety of pathologic states. In recent years it has become clear that a variety of hormones are present in the heart and may participate in the genesis of left ventricular hypertrophy. Our group has demonstrated the synthesis of renin by cultured canine arterial smooth muscle cells and has recently demonstrated the presence of renin and angiotensin II in myocardial cell preparations. Angiotensin II concentration was (+/- standard error of the mean) 4.19 +/- 1.52 pg/10(6) cells. Evidence has been developed to suggest that these components of the renin-angiotensin system are modulatable. These data, taken together with studies from our laboratory and others, raise the distinct possibility that components of the renin-angiotensin system together with catecholamines play a role in the genesis of left ventricular hypertrophy. Recent evidence suggests that the myc proto-oncogene is activated in cells undergoing catecholamine-induced hypertrophy and our laboratory has detected activation of the sis proto-oncogene in at least 1 model of left ventricular hypertrophy. These findings raise the possibility that similar pathogenetic cellular mechanisms operate to produce myocardial hypertrophy, vascular hyperplasia and hypertrophy, and some forms of benign neoplasia. The possible significance of these findings and their relation to peptide hormones and growth factors are discussed.
D000818:Animals; D006332:Cardiomegaly / Q000378:metabolism / Q000503:physiopathology*; D002455:Cell Division; D002478:Cells, Cultured; D005786:Gene Expression Regulation; D006321:Heart / Q000254:growth & development* / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism; D009857:Oncogenes; D051381:Rats; D011921:Rats, Inbred WKY; D012084:Renin-Angiotensin System