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Captopril inhibits ouabain-sensitive Na+/K+-ATPase
R Accetto1, G Rinaldi, A B Weder
1Department of Internal Medicine (Division of Hypertension), University of Michigan Medical Center, Ann Arbor.
Clinical Physiology and Biochemistry
|January 1, 1989
Summary
Captopril inhibits the sodium-potassium pump (Na+/K+-ATPase) in red blood cells and blood vessels. This effect on pump activity may be relevant in physiological studies using high captopril concentrations.
Area of Science:
- Biochemistry
- Pharmacology
- Physiology
Background:
- Captopril is known to inhibit Na+/K+-ATPase activity in erythrocyte membrane fragments.
- The physiological relevance of captopril's effect on Na+/K+ pump activity in intact cells requires further investigation.
Purpose of the Study:
- To investigate the effect of captopril on Na+/K+ pump activity in human erythrocytes and rat tail artery segments.
- To elucidate the mechanism underlying captopril's potential inhibition of Na+/K+-ATPase.
Main Methods:
- Measuring 22Na+ efflux from human erythrocytes to assess Na+/K+ pump activity.
- Evaluating K+-induced relaxation of rat tail artery segments pre-contracted with norepinephrine or serotonin.
- Assessing the impact of captopril on intracellular sodium concentration and other potential mechanisms.
Main Results:
- Captopril demonstrated a concentration-dependent inhibition of 22Na+ efflux from erythrocytes.
- Captopril significantly inhibited ouabain-sensitive Na+/K+ efflux, with 50% inhibition at 2.0 X 10(-3) M.
- Captopril dose-dependently inhibited K+-induced relaxation in rat tail arteries, suggesting vascular smooth muscle Na+/K+-ATPase inhibition.
Conclusions:
- Captopril inhibits membrane Na+/K+-ATPase in both intact red blood cells and vascular smooth muscle cells.
- The precise mechanism of captopril-induced pump suppression remains uncertain.
- Potential inhibition of Na+/K+-ATPase by captopril should be considered in physiological studies employing high drug concentrations.