Effects of captopril (SQ 14, 225) on the renin-angiotensin-aldosterone system in normal rats

Kokubu, Tatsuo; Ueda, Einosuke; Ono, Mototane; Kawabe, Tadao; Hayashi, Yuji; Kan, Takuya

doi:10.1016/0014-2999(80)90094-1

Cited by 52 publications

(10 citation statements)

References 17 publications

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“…The second possibility is that the biosynthesis of ACE in the aorta may be accelerated through the feedback mechanism. As to the elevation of intrinsic ACE activity, it has been already reported that enalapril and captopril increase the ACE activity in the lung and serum after they were administered repeatedly (18)(19)(20)(21), supporting this possibility.…”

Section: Discussionmentioning

confidence: 79%

Pharmacological Studies on TA-6366, a New ACE Inhibitor: II. Effect of Long-Term Administration from the Pre-Hypertensive Stage on Blood Pressure, Relative Heart Weight and ACE Activity of Various Tissues in Spontaneously Hypertensive Rats(SHRs).

et al. 1991

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ABSTRACT-The long-term oral administration of TA-6366 (5 mg/kg/day) from 4 weeks old impeded the genetic hypertension development with only a slight decrease in heart rate in spontaneously hypertensive rats (SHRs). However, the lower dose (1 mg/kg/day) of TA-6366 did not affect the development, but it lowered blood pressure after the development was almost accomplished. Concomitantly, relative heart weights in both the groups were markedly decreased to almost the same degree. The reduc tion of ACE activity in the aorta, brain and lung of both groups was found at 24 hr after the final administration, particularly at the 5 mg/kg/day dose; and that of the aorta was kept at almost the same low level even on the 9th day after withdrawal. Af ter withdrawal of TA-6366 (5 mg/kg/day), the significant decrease in blood pressure was sustained at least for 10 weeks. The beneficial effect of TA-6366 on the hyperten sion development in SHRs seems to be related to its strong and long-lasting ACE in hibition, especially in the vasculature.

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Section: Discussionmentioning

confidence: 79%

Pharmacological Studies on TA-6366, a New ACE Inhibitor: II. Effect of Long-Term Administration from the Pre-Hypertensive Stage on Blood Pressure, Relative Heart Weight and ACE Activity of Various Tissues in Spontaneously Hypertensive Rats(SHRs).

et al. 1991

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“…Standing on the above evidence, we treated rats with captopril which is known to increase the ACE activity in the plasma [13,14] and lung [ 14], and examined whether the activity of ACE in the kidney changes in response to captopril, and identified the area where the change was most prominent.…”

Section: Discussionmentioning

confidence: 99%

Enhancement of Angiotensin-Converting Enzyme Activity in the Inner Cortex of Rat Kidney by Captopril

Song

Tominaga²,

Kanayama³

et al. 1988

Kidney Blood Press Res

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The rat kidney was separated into the outer cortex, inner cortex, outer medulla and inner medulla or papilla, and the distribution of angiotensin-converting enzyme (ACE) in response to consecutive administrations of captopril was studied. In normal animals, the ACE activity in the inner cortex and outer medulla was about 10 and 3 times higher than in the outer cortex, respectively, and the activity in the inner medulla was much the same as that in the outer cortex. Captopril was given in doses of 30 and 100 mg/kg/day for 7 days, and the renal ACE activity on the 8th day was examined. Since it was assumed that the ACE activity might be lower than the full activity when the tissue contained captopril, diamide, a sulfhydryl oxidant, was used to eliminate the effect of any captopril remaining in the tissue extracts. However, this compound at concentrations over 1 mM enhanced the activity of ACE itself to about twice the value when assayed without diamide. Thus, oxidation with sufficient concentrations of diamide resulted in an enhancement of a maximal activity of ACE. When all samples were pretreated with 10 mM diamide and the ACE activity determined, captopril caused a dose-related increase in the ACE activity, but only in the inner cortex. We conclude that ACE locates predominantly in the inner cortex of the rat kidney and it is this area which has an altered ACE activity in response to captopril.

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“…Plasma ACE increases in response to chronic blockade of ACE activity by captopril (1) or enalapril (2) in parallel to the increase of lung ACE, indicating that changes of plasma ACE activity can reflect perturbations of the reninangiotensin system (RAS).…”

Section: Introductionmentioning

confidence: 99%

Changes in Plasma Ace Activity During the Development and Reversal of One-Kidney, One Clip Hypertension in Rats

Santos

Greene

Krieger

1989

Clinical and Experimental Hypertension. Part A: Theory and Prac

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Plasma angiotensin converting enzyme (ACE) activity was studied during the development and the reversal of one-kidney, one clip (1K1C) renal hypertension in rats (RHR). Plasma ACE activity was measured in RHR 1 (n = 11), 3 (n = 8), 6 (n = 12), 14 (n = 7), and 80-120 days (n = 17) after clipping. Plasma ACE activity (nmol/min/ml) was elevated (p less than 0.05) in chronic RHR (80-120 days; mean arterial pressure, MAP: 216 +/- 9 mmHg), being 142 +/- 14 (n = 17) vs. 100 +/- 3.2 (n = 20) for normotensive control rats (MAP: 116 +/- 3 mmHg), whereas no significant differences were observed at earlier times. Overactivity of the renin-angiotensin system (RAS) was demonstrated indirectly by the reduction of MAP (greater than 15 mmHg) in response to captopril (10 mg/kg, i.v.) only during the first 3 days after clipping and in chronic severely hypertensive rats. In another experiment, ACE activity in chronic RHR was measured serially before and 1, 6 and 24 hours after unclipping. Serial measurements of plasma ACE showed a progressive decrease from 145 +/- 26 to 122 +/- 21, 24 hours after unclipping (n = 7, p less than 0.05, paired Student t-test) when MAP was reduced from 204 +/- 15 to 113 +/- 7 mmHg. There was essentially no change during 24 hours from the initial values of RHR-sham (MAP: 206 +/- 5 mmHg, ACE: 140 +/- 19, n = 8) and normal rats-sham (MAP: 115 +/- 2 mmHg, ACE: 96 +/- 3, n = 6). These data provide further evidence that chronic renal hypertension is associated with important changes in the metabolism of vasoactive peptides.

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Effects of captopril (SQ 14, 225) on the renin-angiotensin-aldosterone system in normal rats

Cited by 52 publications

References 17 publications

Pharmacological Studies on TA-6366, a New ACE Inhibitor: II. Effect of Long-Term Administration from the Pre-Hypertensive Stage on Blood Pressure, Relative Heart Weight and ACE Activity of Various Tissues in Spontaneously Hypertensive Rats(SHRs).

Pharmacological Studies on TA-6366, a New ACE Inhibitor: II. Effect of Long-Term Administration from the Pre-Hypertensive Stage on Blood Pressure, Relative Heart Weight and ACE Activity of Various Tissues in Spontaneously Hypertensive Rats(SHRs).

Enhancement of Angiotensin-Converting Enzyme Activity in the Inner Cortex of Rat Kidney by Captopril

Changes in Plasma Ace Activity During the Development and Reversal of One-Kidney, One Clip Hypertension in Rats

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