| Budget Amount *help |
¥14,500,000 (Direct Cost: ¥14,500,000)
Fiscal Year 2006: ¥7,000,000 (Direct Cost: ¥7,000,000)
Fiscal Year 2005: ¥7,500,000 (Direct Cost: ¥7,500,000)
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| Research Abstract |
The heart is a pump organ; however, it might produce many hormones in heart failure. Especially ANP and BNP are synthesized in large quantities. We have recently shown that various kinds of steroid hormone are also synthesized with a very small quantity. On the other hand, the action of steroid hormones in the heart may also exceed the conventional concept. In this study, we found that aldosterone has an action for anti-cellular dehydration; Na^+/H^+ exchanger 1 (NHE1) plays an important role there deeply. Cell shrinkage under high osmolarity was prevented by making Na^+ flow into the cell. However, when this became a long period, the rise of intracellular Ca^<2+> concentration leaded to cardiac hypertrophy.
From the clinical side, we advanced researches on the medical treatment of heart failure. Although the inhibitory drugs of the renin-angiotensin system and anti-aldosterone agents are indispensable, too much rise of the potassium concentration is an important problem. We examined in detail what kind of factors would influence the potassium concentration by using 1,035 patients admitted to our institution. As a result, although renal insufficiency, diabetes, and use of the inhibitory drugs of the RAA system raised the potassium concentration, it was reduced rather in heart failure status. This is contrary to the conventional research findings; and thus the further argument is needed. On the other hand, although hANP is used more often in acute heart failure, there are still unknown mechanisms. In this study, we divided the heart failure patients into two groups; hANP treatment group and furosemide treatment group. Although the improvement of hemodynamic parameters were almost similar, the improvement of oxidative stress was significantly lager in the hANP group. This action will be confirmed also in the experiment using cultured neonatal rat cardiomyocyte, and the elucidation of that mechanism is a future subject.
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