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Platelet membrane Ca(2+)-ATPase: blunted calmodulin-stimulation in essential hypertension
T J Resink1, V A Tkachuk, P Erne
1Department of Research, University Hospital, Basel, Switzerland.
Summary
Platelets in essential hypertension show impaired calmodulin-stimulated calcium pump activity, suggesting a failure in calcium homeostasis despite increased pump capacity. This may be an adaptation to higher intracellular calcium levels.
Area of Science:
- Biochemistry
- Cardiovascular Physiology
Background:
- Essential hypertension is linked to calcium dysregulation.
- Platelets are implicated in cardiovascular disease and calcium homeostasis.
Purpose of the Study:
- To investigate if defective calcium-efflux pump activity causes calcium overload in hypertensive platelets.
- To compare calmodulin-stimulated Ca(2+)-ATPase in normotensive and hypertensive subjects.
Main Methods:
- Compared calmodulin-stimulated Ca(2+)-ATPase in platelet membranes from 25 normotensive and 27 hypertensive individuals.
- Assessed enzyme affinity for calmodulin and Ca2+.
- Measured basal and calmodulin-activated Ca(2+)-ATPase activity.
Main Results:
- No difference in Ca(2+)-ATPase affinity for calmodulin or Ca2+ between groups.
- Diminished calmodulin-stimulation of Ca(2+)-ATPase activity in hypertensive patients (64%) vs. normotensive subjects (125%) (P < 0.01).
- Markedly greater Ca(2+)-ATPase capacity (1.5-1.8 fold) in hypertensive platelet membranes (both native and calmodulin-deficient).
Conclusions:
- Calmodulin-stimulation of platelet Ca(2+)-ATPase is less effective in essential hypertension.
- Increased Ca(2+)-ATPase capacity in hypertensive platelets may be an adaptive response to elevated intracellular calcium.
- Defective calcium efflux contributes to calcium overload in hypertension.