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Related Experiment Videos

Does captopril reduce renal function in renovascular disease by postglomerular vasodilatation?

G Schwietzer, C Laass, D Kampf

    Journal of Hypertension. Supplement : Official Journal of the International Society of Hypertension
    |November 1, 1985
    PubMed
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    Angiotensin converting enzyme (ACE) inhibitors can decrease kidney function in patients with transplant renal artery stenosis (TRAS). This study found that reduced glomerular filtration rate (GFR) after ACE inhibition in TRAS patients may not be due to postglomerular vasodilation.

    Area of Science:

    • Nephrology
    • Hypertension
    • Pharmacology

    Background:

    • Renal artery stenosis (RAS) can cause decreased kidney function after ACE inhibitor administration.
    • This effect is often attributed to efferent arteriolar vasodilation.
    • The hypothesis needs further investigation in specific patient populations.

    Purpose of the Study:

    • To investigate the mechanism of glomerular filtration rate (GFR) decrease after captopril administration in hypertensive patients with and without transplant renal artery stenosis (TRAS).
    • To determine if acute postglomerular vasodilation occurs following ACE inhibition in TRAS patients with a high-renin state.

    Main Methods:

    • Acute changes in mean arterial pressure (MAP), renal plasma flow (RPF), GFR, plasma renin activity (PRA), and PGE2-excretion were measured after oral captopril administration.

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  • Patients included hypertensives with and without TRAS, treated with diuretics.
  • Hemodynamic and renal function parameters were compared between groups.
  • Main Results:

    • GFR decreased significantly in both TRAS and non-TRAS groups after captopril.
    • No evidence of postglomerular vasodilation was observed in the TRAS group.
    • Filtration fraction decreased only in patients without TRAS; PRA and PGE2-excretion showed no significant changes between groups.
    • A severe TRAS patient experienced comparable GFR decrease with both ACE inhibition and sodium nitroprusside.

    Conclusions:

    • Acute postglomerular vasodilation does not necessarily explain the GFR decrease after ACE inhibition in TRAS patients with high-renin states.
    • The findings challenge the prevailing hypothesis regarding the mechanism of renal dysfunction following ACE inhibition in this specific patient group.
    • Further research is needed to fully elucidate the complex mechanisms involved.