Kinetic Studies of the Pharmacologic Response to Captopril in Rats. II. Hypotensive Effect and Plasma Angiotensin Converting Enzyme Activity
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概要
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The effect of captopril on the mean arterial blood pressure was studied in rats. Two different disease-state rats, namely the sodium-deficient rat (SDR) and the two-kidney-one-clip Goldblatt hypertensive rat (GHR), as well as normotensive rats (NR), were used. After i.v. bolus administration of captopril to each rat, the time course of plasma angiotensin converting enzyme (ACE) activity and mean arterial blood pressure were determined. In a different experiment, the effect of captopril on the plasma ACE activity in vitro was determined. Captopril inhibited the plasma ACE activity in a concentration-dependent manner and the relationship between concentration of captopril and inhibition of plasma ACE activity in vitro was reasonably described by a Langmuir-type equation. Then, plasma concentrations of captopril after i.v. administration were estimated by means of this equation. The estimated plasma concentration of captopril followed a double exponential equation. From the data obtained, a kinetic model including the renin-angiotensin system and pharmacokinetics of captopril was constructed under the following assumptions ; (1) the hypotensive effect of captopril is solely attributable to the reduction of angiotensin II level in the body, (2) the production rate of angiotensin II is proportional to the total ACE activity and (3) plasma ACE activity reflects the total ACE activity in the body. Then, the effect of captopril on the mean arterial blood pressure in each type of rat was calculated. The results indicated that the hypotensive effect of captopril in NR was reasonably described by the model. However, the hypotensive effect of captopril in both GHR and SDR could not be well described by the model. These facts indicate that the decrease in mean arterial pressure in response to captopril may be due to a combination of decreased circulating levels of angiotensin II and an angiotensin-independent mechanism such as the kallikrein-kinin system, at least in the high-renin condition.
- 社団法人日本薬学会の論文
- 1989-09-01
著者
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KATAYAMA Kazunori
Faculty of Pharmaceutical Sciences, Toyama Medical and Pharmaceutical University
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KAKEMI Masawo
Faculty of Pharmaceutical Sciences, Toyama Medical and Pharmaceutical University
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KOIZUMI Tamotsu
Faculty of Pharmaceutical Sciences, Toyama Medical and Pharmaceutical University
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ENDOH Makiko
Faculty of Pharmaceutical Sciences, Toyama Medical and Pharmaceutical University
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Koizumi T
Toyama Medical & Pharmaceutical Univ. Toyama Jpn
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Endoh Makiko
Faculty Of Pharmaceutical Sciences Toyama Medical And Pharmaceutical University
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Endoh Makiko
富山医科薬科大学 薬
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Katayama K
Toyama Medical And Pharmaceutical Univ. Toyama Jpn
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Katayama K
Faculty Of Pharmaceutical Sciences Toyama Medical And Pharmaceutical University
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Kakemi Masawo
Faculty Of Pharmaceutical Sciences Toyama Medical And Pharmaceutical University
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Kakemi M
Department Of Pharmaceutics Osaka University Of Pharmaceutical Sciences
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Kakemi Masao
大阪薬科大学 薬剤学
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SUZUKI Masahiro
Faculty of Pharmaceutical Sciences, Toyama Medical and Pharmaceutical University
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Koizumi T
Toyama Medical And Pharmaceutical Univ. Toyama Jpn
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Katayama Kazunori
Faculty Of Pharmaceutical Science Toyama Medical And Pharmaceutical University
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Kakemi M
Osaka Univ. Pharmaceutical Sci. Osaka Jpn
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Koizumi Tamotsu
Faculty Of Pharmaceutical Science Toyama Medical And Pharmaceutical University
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Kakemi M
Osaka Univ. Pharmaceutical Sci. Takatsuki Jpn
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Suzuki Masuko
Department Of Microbiology Tohoku Pharmaceutical University
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Suzuki M
Faculty Of Pharmaceutical Sciences Toyama Medical And Pharmaceutical University
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Kakemi M
Faculty Of Pharmaceutical Sciences Toyama Medical And Pharmaceutical University
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Suzuki Masahiro
Faculty Of Engineering Ibaraki University
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