アンジオテンシンI変換酵素阻害剤captoprilの臓器ならびに血漿カテコールアミン濃度に及ぼす影響

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Two studies were designed to examine the effect of the angiotensin converting enzyme inhibitor, captopril, on the sympathetic nervous system. In the first study, blood pressure (BP), heart rate (HR), and norepinephrine (NE) concentrations in the heart were measured in rats which had been given the agent orally in tap water (0.5mg/ml) for 2, 9, 19, 29, and 58 days. BP and HR were measured using a tail-microphone to which a tachometer to record HR was connected in the unanesthetized and unrestricted condition. Heart NE was extracted with perchrolic acid and measured with the THI method on a high pressure liquid chromatography. The same study was also done in the control rats. The BP of the rats which had been given captopril for 9 days or more was significantly lower than in the control rats, while HR was not different between the two groups of rats. The ratio of heart weight/body weight was significantly lower in the captopril rats than in the control rats 58 days after the captopril administration. The ratio was significantly correlated with BP in these captopril and control rats (r=0.59, p<0.01). In contrast to the control rats, the NE concentrations in the heart gradually increased in the captopril rats, thus being significantly higher in the latter than in the former after 29 and 58 days of captopril administration (p<0.01 for both observations).In addition, the lower the BP was, the higher the NE concentrations in the heart was in all the rats (r=-0.52, p<0.001). In the second study, BP, HR, and NE concentrations in plasma, heart, brain and the left kidney were measured in rats which had been on captopril for 2 and 29 days. Renal renin content (RRC) was also measured in the right kidney. In this study, BP and HR were recorded through a carotid catheter which had been inserted 4 hrs previously under light ether anesthesia. BP was significantly lower and NE concentrations in the heart was higher in the captopril rats than in the control rats after 29 days of captopril administration. There was a significant negative correlation between BP and NE concentrations in the heart in the captopril and the control rats (r=-0.88, p<0.001). No difference in HR was found between the 2 groups. NE concentrations in plasma, brain and kidney showed no significant differences between the captopril and the control rats in either of the stages of sacrifice. RRC was markedly reduced in the rats with 2 days of captopril, while it increased in the rats with 29 days of captopril. However, the RRC had no definite relationship with the NE concentrations in plasma or that in the kidney. The results show that chronic administration of captopril reduces the heart weight in normotensive rats. This effect points on the one hand to a decrease in "cardiac after-load" and on the other to changes of humoral factors such as plasma angiotensin II induced by captopril. The increase in NE concentrations in the heart in the captopril rats is considered to be due mainly to an activated sympathetic nervous function caused by the decrease in BP, since there was a significant negative correlation between BP and NE concentrations in the heart. However, in spite of the decrease in BP, the HR and the NE concentrations in plasma, brain, and kidney in the captopril rats were not different from those in the control rats. Thus, it is suggested that captopril may somehow suppress sympathetic nervous function, and that this effect may participate in, in part, to the decrease in BP. Furthermore, the changes in RRC in the captopril rats had no definite relationship with those in the NE concentrations in plasma and kidney. The role of the sympathetic nervous system in the changes of RRC which were observed in the captopril rats remains to be clarified.
日本内分泌学会の論文

アンジオテンシンI変換酵素阻害剤captoprilの臓器ならびに血漿カテコールアミン濃度に及ぼす影響

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