Mechanisms of the cardiac/vasculor hypertrophy and cardio-protection

点击翻译按钮获取中文摘要

1) Angiotensin converting enzyme (ACE) increased markedly in the infarct area and modetately in hypertrophied myocardium without changing the affinity compared to the sham-operated rats. The study confirms that cardiac ACE may participate in the pathophysiology of cardiac hypertrophy in chronic heart failure.2) We investigated the actions of f-Met-Leu-Phe (FMLP) and its cellular mechamism in human coronary arteries. A reverse transcription-polymerase chain reaction (RT-PCR) showed predominent expression of FMLP receptor homologues, FPRH1 and FPRH2 mRNA,in human coronary medial tissue relative to that in leukocytes.3) We assessed the renal-protective effect of long-acting antihypertensive drugs (losartan 5 mg/kg/day p.o., imidapril 5 mg/kg/day p.o., amlodipine 5 mg/kg/day p.o. ; in drinking solution for 12 weeks) in rats with chronic renal failure. The results indicate that these long-acting antihypertensive drugs equally have potency to protrct heart and kidney in rats with CRF.They also indicate that the kallikrein-kinin system might not play a major role in the cardio-and reno-protective effects of ACE inhibitors in rats with CRF.4) Chronic administration of a specific endothelin subtype A receptor antagonist, FR139317 (32 mg/kg/day i.p.) and an angiotensin converting enzyme inhibitor, enalapril (2mg/kg/day i.p.), in combination with moderate exercise were investigated in rats with chronic renal failure. Moderate exercise may protect renal function in this model. They also suggest that FR139317 may not have an additional antihypertensive and renal protective effect in this exercise model.