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Angiotensin-converting enzyme inhibition, catecholamines and hemodynamics in essential hypertension
Insights
Captopril effectively lowers blood pressure in patients with essential hypertension by reducing total peripheral resistance. This angiotensin-converting enzyme inhibitor did not significantly alter sympathetic nervous system activity.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Essential hypertension is a widespread cardiovascular condition.
- Angiotensin-converting enzyme (ACE) inhibitors represent a key therapeutic class.
Purpose of the Study:
- To evaluate the hemodynamic and neurohormonal effects of captopril in patients with essential hypertension.
- To determine the mechanism of blood pressure reduction by captopril.
Main Methods:
- 15 patients with essential hypertension (WHO II) received captopril (300-600 mg/day) for 8 weeks.
- Hemodynamic parameters (thermodilution) and plasma levels of norepinephrine, epinephrine, renin activity, and aldosterone were measured.
- Measurements were taken after placebo and captopril treatment.
Main Results:
- Captopril significantly reduced systolic and diastolic arterial pressures in both supine and standing positions.
- A significant correlation was found between blood pressure decrease and reduced total peripheral resistance.
- Cardiac index remained unchanged, while stroke index increased due to a heart rate decrease.
- Plasma catecholamines and their response to posture were unaffected; plasma renin activity increased, and aldosterone decreased.
Conclusions:
- Captopril lowers arterial pressure primarily by reducing total peripheral resistance, suggesting ACE inhibition as the main mechanism.
- The study found no evidence of significant reduction in sympathetic nervous system activity with captopril treatment.
- Captopril is an effective antihypertensive agent for essential hypertension, acting via the renin-angiotensin system modulation.
Abstract:
Captopril was given to 15 unselected patients with essential hypertension (WHO II) at a dose range of 300 to 600 mg/day. Hemodynamic indexes (thermodilution) as well as levels of plasma norepinephrine, epinephrine, renin activity and aldosterone were determined simultaneously at the end of 2 weeks of placebo and after 8 weeks of captopril treatment. Systolic and diastolic arterial pressures were reduced significantly by treatment both supine (p less than 0.0025) and standing (p less than 0.0025). The diastolic arterial pressure was normalized (less than 95 mm Hg) in five patients and significantly reduced in four, whereas six patients were considered poor responders (mean arterial pressure decrease 10 mm Hg or less). The decrease in arterial pressure correlated significantly with the reduction in total peripheral resistance (r = 0.71), whereas cardiac index did not change and stroke index increased because of a slight decrease of heart rate. Plasma and urinary norepinephrine and epinephrine did not change during treatment. Moreover, the response of both heart rate and plasma catecholamines to upright posture was not altered by captopril treatment. Plasma renin activity increased and plasma aldosterone concentration decreased during treatment. These results suggest that inhibition of converting enzyme activity by captopril induces a reduction in arterial pressure through a reduction in total peripheral resistance. There was no evidence of an appreciable reduction in sympathetic nervous system activity during therapy.