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Captopril, aldosterone and urinary kallikrein in primary hypertension
Insights
Captopril effectively lowers blood pressure in hypertensive patients by reducing aldosterone and angiotensin II. Further research is needed to understand the renal kallikrein-kinin system’s role.
Area of Science:
- Cardiology
- Pharmacology
- Nephrology
Background:
- Primary hypertension affects millions globally.
- The renin-angiotensin-aldosterone system (RAAS) and kallikrein-kinin system (KKS) play crucial roles in blood pressure regulation.
- Captopril is an angiotensin-converting enzyme (ACE) inhibitor used to treat hypertension.
Purpose of the Study:
- To investigate the effects of captopril on blood pressure, RAAS, and KKS in patients with primary hypertension.
- To assess the impact of adding hydrochlorothiazide when blood pressure targets are not met.
- To explore correlations between hormonal changes and blood pressure reduction.
Main Methods:
- 32 patients with primary hypertension (WHO stage I-II) received captopril.
- Hydrochlorothiazide was added as needed to achieve target blood pressure.
- A placebo control group (n=8) was included for comparison.
- Measurements included blood pressure, plasma aldosterone, plasma angiotensin II, 24-h urinary aldosterone, and 24-h urinary kallikrein.
Main Results:
- Captopril significantly reduced mean arterial pressure, plasma aldosterone, 24-h urinary aldosterone, plasma angiotensin II, and 24-h urinary kallikrein.
- Blood pressure reduction correlated with pretreatment plasma renin activity (PRA).
- Hydrochlorothiazide further lowered blood pressure but increased plasma aldosterone and 24-h urinary kallikrein.
- Hydrochlorothiazide alone increased 24-h urinary aldosterone.
Conclusions:
- Captopril effectively modulates the RAAS and KKS in hypertensive patients.
- The study suggests additional regulatory mechanisms for the renal KKS beyond aldosterone and renal arterial pressure.
- Understanding these complex interactions is vital for optimizing hypertension management.
Abstract:
The effects on blood pressure, the renin-angiotensin-aldosterone and the kallikrein-kinin systems were investigated in 32 patients with primary hypertension WHO stage I-II treated with captopril. Hydrochlorothiazide was added if needed to achieve a supine diastolic blood pressure of less than or equal to 90 mmHg. A placebo control group (n=8) was treated similarly. Supine mean arterial pressure fell from 133 +/- 10 on placebo to 114 +/- 12 mmHg after 4 weeks on captopril. At the same time plasma aldosterone decreased from 263 +/- 188 to 164 +/- 101 pmol . 1(-1), 24 h urinary excretion of aldosterone from 18 +/- 12 to 12 +/- 10 nmol and kallikrein from 9.0 +/- 6.7 to 6.2 +/- 4.1 nkat. Plasma angiotensin II was significantly reduced after two weeks treatment from 23.2 +/- 8.6 to 17.0 +/- 6.7 pmol . 1(-1). Before, but not during captopril, 24 h urinary kallikrein excretion correlated with plasma aldosterone levels and 24 h urinary aldosterone excretion (r=0.44 p, less than 0.05 and r=0.53, p less than 0.01, respectively). Mean arterial pressure reduction on captopril correlated with pretreatment PRA (r=0.44, p less than 0.05) but not with other measured hormone levels or changes therein. The addition of hydrochlorothiazide caused a further fall in blood pressure, but increased plasma aldosterone and 24 h urinary kallikrein excretion. Hydrochlorothiazide alone increased only 24 h urinary aldosterone excretion significantly. These findings indicate that, besides aldosterone secretion and renal arterial pressure, further mechanisms regulating the release of and activity of the renal kallikrein-kinin system exist.