| Co-Investigator(Kenkyū-buntansha) |
田辺 一明 島根医科大学, 医学部, 医員
MATSUNO Yoshio Shimane Medical University, 医学部, 助手 (90144708)
MORIOKA Shigefumi Shimane Medical University, 医学部, 助教授 (00157877)
MORIYAMA Katsutoshi Shimane Medical University, 医学部, 教授 (10034919)
TANABE Kazuaki Shimane Medical University
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| Research Abstract |
Cardiac hypertrophy is a commom complication of arterial hypertension, but its pathogenesis is not well understood. Previous studies have suggested that left ventricular hypertrophy in hypertension is an adaptive and compensatory response by the heart to increased afterload and that the extent of hypertrophy can be directly correlated with the severity of hypertension. However, recent extensive studies have revealed that this is not true in all cases, and that factors which initiate and develop cardiac hypertrophy differ according to the type of hypertension. Recent studies also have suggested that some humoral factors other than catecholamine and renin-angiotensin II may contribute to the development of cardiac hypertrophy. In the present study, therefore, we investigated the possibility of the existence of humoral factor(s) which induce and/or modulate cardiac hypertrophy in perinephritic hypertension induced by the Page method. To investigate such humoral factors, a microassay syste
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m inevitably necessary, so we established such assay system using cultured rat heart cells at first. When the usefulness of this assay system was investigated by using catecholamine which is well known to induce cardiac hypertrophy, this assay system was found to be very useful for such purpose. The potential ability of angiotensin II for organ hypertrophy is one of the recent topic of cardiovascular diseases. Our present study revealed that angiotensin II can directly act on cultured heart cells, thereby stimulates protein metabolism of cultured rat heart cells. The main purpose of this study was to investigate whether or not there exists some humoral factor(s) which induce cardiac hypertrophy in perinephritic hypertension in dogs. Our results in the present study showed that heart extract obtained from hypertrophied, left ventricle of perinephritic hypertension in dogs increased the uptake of ^3H-uridine and ^<14>C-leucine into cultured heart cells. After partial purification of this factor by a gel filtration technique and a HPLC system, we also found that a molecule with molecular weight about 11200 has an ability to stimulate protein metabolism of cultured heart cells. Furthermore our preliminary results suggest that thi factor is heat labile and that the activity of this factor has been lost after treatment with proteolytic enzyme, trypsin, thereby suggesting that this factor may be a kind of peptide or protein. The pathophysiological role of this stumulatory factor is still unknown, but it may control biochemical events involved in the development of cardiac hypertrophy. We are now attempting to further purify and characterize this stimulatory factor and shed light on its pathophysiological role in cardiac hypertrophy in this model of hypertension. Less
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