Why the study?
Does partial genetic deficiency in tissue kallikrein activity (R53H polymorphism) affect vascular, hormonal, and renal phenotypes in young normotensive males under varying dietary sodium and potassium conditions?
Population
40 young normotensive white males (30 R53R-homozygous and 10 R53H-heterozygous for the tissue kallikrein gene)
Comparison
Low sodium-high potassium diet and high… vs Crossover design comparing the two diets, as…
Design
RCT, Randomly assigned to receive both diets in a crossover design
Follow-up
2 weeks (1 week per diet)
Authors
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R53H carriers may face elevated long-term vascular risk despite normotension; extends tissue kallikrein’s role to human arterial structure.
Does partial genetic deficiency in tissue kallikrein activity (R53H polymorphism) affect vascular, hormonal, and renal phenotypes in young normotensive males under varying dietary sodium and potassium conditions?
Partial genetic deficiency in tissue kallikrein activity is associated with inward remodeling of the brachial artery and increased wall shear stress, representing a novel form of arterial dysfunction.
Azizi et al. (2005) studied this question.
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