[Captopril in the treatment of arterial hypertension in chronic nephritis]
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Captopril effectively lowers high blood pressure in chronic glomerulonephritis patients. This medication improves renal blood flow and reduces vascular resistance with minimal side effects.
Area of Science:
- Nephrology
- Cardiovascular Medicine
- Pharmacology
Context:
- Chronic glomerulonephritis frequently leads to arterial hypertension.
- The renin-angiotensin-aldosterone system plays a crucial role in regulating blood pressure and renal function.
Purpose:
- To investigate the effects of captopril on arterial pressure, renal function, and related regulatory factors in patients with chronic glomerulonephritis and hypertension.
Summary:
- Captopril significantly reduced hypertension regardless of baseline renin-angiotensin-aldosterone system activity.
- Prolonged captopril use increased renal blood flow and decreased renal vascular resistance, with a transient dip in glomerular filtration initially.
- The drug increased blood renin activity, decreased aldosterone, and enhanced renal prostaglandin synthesis, while potassium excretion decreased and blood levels rose.
Impact:
- Captopril demonstrates a favorable safety profile and efficacy in managing hypertension associated with chronic glomerulonephritis.
- The findings elucidate captopril's multifaceted mechanisms of action on both systemic blood pressure and intrarenal hemodynamics.
Abstract:
The effect of captopril on arterial pressure, indices of renal function and renal function regulating factors was studied in 13 patients suffering from chronic glomerulonephritis with arterial hypertension. Captopril considerably decreased the expression of hypertension irrespective of the initial status of the renin-angiotensin-aldosterone system. A prolonged use of captopril resulted in an increase in the renal blood flow, a considerable decrease in the resistance of the renal vessels. A transient decrease in a glomerular filtration value was noted on the first days of treatment. The use of captopril did not cause significant changes in sodium balance; potassium excretion with urine decreased, its concentration in the blood increased. Captopril caused a sharp increase in the blood renin activity, a decrease in aldosterone production and excretion and an increase in the synthesis of renal prostaglandins. Captopril was well tolerated by the patients, noticeable side effects were undetectable. Mechanisms of the hypotensive effect of the drug and mechanisms of its action on renal function were discussed.