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Platelet calcium transport in hypertension
W L Dean1, J E Pope, M E Brier
1Department of Biochemistry, University of Louisville School of Medicine, KY 40292.
Hypertension (Dallas, Tex. : 1979)
|January 1, 1994
Summary
In hypertension, reduced plasma membrane calcium ATPase (Ca2+-ATPase) activity in platelets may elevate cytosolic calcium. This finding highlights a potential mechanism contributing to platelet dysfunction in high blood pressure.
Area of Science:
- Cardiovascular Physiology
- Cellular Biology
- Biochemistry
Background:
- Elevated cytosolic calcium in platelets is implicated in hypertension.
- Platelet calcium transport mechanisms require further elucidation in hypertensive individuals.
Purpose of the Study:
- To identify specific platelet calcium (Ca2+) transport proteins linked to increased cytosolic Ca2+ in hypertension.
- To investigate the relationship between blood pressure and Ca2+ transporters in platelet membranes.
Main Methods:
- Utilized thapsigargin to differentiate between plasma and internal membrane Ca2+-ATPases.
- Assayed inositol 1,4,5-trisphosphate-mediated and Ca2+ ionophore-induced Ca2+ release using rhod-2.
- Measured glycoprotein IIIa levels via immunoblotting.
Main Results:
- Plasma membrane Ca2+-ATPase activity significantly decreased with increasing diastolic blood pressure (P < .002).
- Internal membrane Ca2+-ATPase activity showed no significant correlation with blood pressure or age.
- Inositol trisphosphate-mediated Ca2+ release negatively correlated with age (P < .024), but not blood pressure.
Conclusions:
- Reduced plasma membrane Ca2+-ATPase activity in platelets is associated with hypertension.
- This inhibition may directly lead to elevated cytoplasmic Ca2+ and enhanced platelet sensitivity.
- Findings suggest a novel mechanism for platelet hyper-reactivity in hypertensive states.