What question did this study set out to answer?

To clarify the mechanisms driving the blood pressure-lowering effect of captopril by examining its acute and chronic impacts on the kallikrein-kinin and renin-angiotensin systems.

January 1, 1986Japanese Journal of MedicineOpen Access

The mechanism of the hypotensive effect of captopril (converting enzyme inhibitor) with special reference to the kallikrein-kinin and renin-angiotensin systems.

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Why the study?

Does captopril reduce blood pressure and alter the kallikrein-kinin and renin-angiotensin systems in patients with hypertension?

Population

33 in-patients with hypertension, free from overt renal dysfunction, off antihypertensive drugs for at least…

Design

Cohort

Follow-up

14 days

Authors

OIOsamu IimuraSapporo Medical University KSKazuaki ShimamotoPreventive Cardiology STShigemichi TanakaTeine Keijinkai Hospital

Discussion

Member takes

Implication

Captopril-associated BP reduction may involve kinin elevation in hypertension; hypothesis-generating for dual mediation, needing RCTs before practice change.

Key Points

To clarify the mechanisms driving the blood pressure-lowering effect of captopril by examining its acute and chronic impacts on the kallikrein-kinin and renin-angiotensin systems.
Evaluated acute drug effects following a single 50 mg oral dose of captopril in 14 patients with hypertension.
Evaluated chronic drug effects following daily oral administration of 75–300 mg of captopril for 14 days in 19 patients with hypertension.
Measured changes in blood pressure, heart rate, plasma renin activity, plasma angiotensin II, blood kinins, urinary kinin excretion, urinary kallikrein, and sodium excretion.
Acute administration significantly lowered blood pressure from 30 minutes to a maximum reduction at 60–180 minutes without altering heart rate, while increasing blood kinins and plasma renin activity and decreasing plasma angiotensin II.
Chronic 14-day administration maintained similar reductions in blood pressure and angiotensin II alongside elevated blood kinins, plasma renin activity, urine volume, and urinary sodium excretion.
Blood pressure reductions correlated negatively with baseline plasma renin activity, baseline angiotensin II, and kinin increases, while correlating positively with decreases in plasma angiotensin II.

Structured PICO

Does captopril reduce blood pressure and alter the kallikrein-kinin and renin-angiotensin systems in patients with hypertension?

Population

33 in-patients with hypertension (14 for acute study: 12 essential, 2 renovascular, age 19-62, 9 men/5 women; 19 for chronic study: essential hypertension, age 19-75, 10 men/9 women), free from overt renal dysfunction, off antihypertensive drugs for at least 14 days.

Intervention

Captopril (50 mg once orally for acute effect; 75-300 mg daily for 14 days for chronic effect)

Outcome

Changes in blood pressure, blood kinin levels, plasma renin activity (PRA), and plasma angiotensin II levelssurrogate

The hypotensive effect of captopril is mediated not only by decreased angiotensin II but also by increased blood kinin levels, urine volume, and urinary sodium excretion.

Cite This Study

Iimura et al. (1986) studied this question.

synapsesocial.com/papers/6a916e4e8c4797ddb5a15e8d https://doi.org/10.2169/internalmedicine1962.25.34

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Implication

Captopril-associated BP reduction may involve kinin elevation in hypertension; hypothesis-generating for dual mediation, needing RCTs before practice change.

The mechanism of the hypotensive effect of captopril (converting enzyme inhibitor) with special reference to the kallikrein-kinin and renin-angiotensin systems.

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

The mechanism of the hypotensive effect of captopril (converting enzyme inhibitor) with special reference to the kallikrein-kinin and renin-angiotensin systems.

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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