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Many membrane abnormalities in hypertension result from one primary defect.
D F Bohr1, P B Furspan, A F Dominiczak
1Department of Physiology, University of Michigan, School of Medicine, Ann Arbor 48109.
Advances in Experimental Medicine and Biology
|January 1, 1991
Summary
Hypertension may stem from inherent abnormalities in the cell
Area of Science:
- Biochemistry
- Cell Biology
- Physiology
Background:
- Integral membrane protein function is sensitive to lipid bilayer changes.
- Reduced calcium binding to plasma membranes is observed in hypertension.
- Genetic hypertension is associated with lipid bilayer structural and functional defects.
Purpose of the Study:
- To investigate the hypothesis that hypertension-related membrane transport abnormalities originate from intrinsic lipid bilayer defects.
Main Methods:
- Review of existing evidence on lipid bilayers and membrane proteins.
- Analysis of calcium binding in hypertensive models.
- Examination of structural and functional properties of lipid bilayers in genetic hypertension.
Main Results:
- Evidence supports that lipid bilayer alterations impact membrane protein function.
- Hypertension is linked to decreased plasma membrane calcium.
- Structural and functional abnormalities of the lipid bilayer are documented in genetic hypertension.
Conclusions:
- Multiple membrane transport system dysfunctions in hypertension are proposed to be secondary to inherent lipid bilayer abnormalities.
- The lipid bilayer's integrity is crucial for proper function of resident transport proteins.