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http://purl.uniprot.org/citations/18327081http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/18327081http://www.w3.org/2000/01/rdf-schema#comment"

Objectives

Tissue kallikrein is a major kinin-forming enzyme involved in artery and kidney functions. Urinary tissue kallikrein activity (UKLKa) reflects renal tissue kallikrein activity and depends on Na and K intake, and genetic factors, especially the tissue kallikrein-inactivating polymorphism, R53H. The effect of these factors on the level of kinin peptides is, however, not known. Moreover, a circulating form of tissue kallikrein is present in human plasma but its origin and regulation are unknown.

Methods

We used a crossover study to investigate UKLKa, plasma tissue kallikrein (pTK), and urinary kallidin peptides and metabolites (Uki) in 10 R53H and 30 R53R normotensive male subjects randomly assigned to either a 1-week low Na-high K or a high Na-low K diet.

Results

UKLKa was 50-60% lower in R53H than R53R subjects and was increased by the low Na-high K diet. pTK was also 45-55% lower in R53H than R53R subjects and was increased by the low Na-high K diet. Uki was slightly but significantly higher under the low Na-high K than the high Na-low K diet, but did not differ between genotypes.

Conclusion

These observations indicate that pTK levels are genetically determined and regulated by Na and K diet, in parallel with UKLKa; this suggests that circulating tissue kallikrein originates mainly from the kidney, and can contribute to circulatory adaptation to dietary ions. Uki is influenced by the Na and K diet, suggesting that kinins participate in renal adaptation to ion intake, but do not quantitatively reflect tissue kallikrein activity in urine, or presumably, in the kidney."xsd:string
http://purl.uniprot.org/citations/18327081http://purl.org/dc/terms/identifier"doi:10.1097/hjh.0b013e3282f4d1fa"xsd:string
http://purl.uniprot.org/citations/18327081http://purl.uniprot.org/core/author"Alhenc-Gelas F."xsd:string
http://purl.uniprot.org/citations/18327081http://purl.uniprot.org/core/author"Azizi M."xsd:string
http://purl.uniprot.org/citations/18327081http://purl.uniprot.org/core/author"Campbell D.J."xsd:string
http://purl.uniprot.org/citations/18327081http://purl.uniprot.org/core/author"Emanueli C."xsd:string
http://purl.uniprot.org/citations/18327081http://purl.uniprot.org/core/author"Peyrard S."xsd:string
http://purl.uniprot.org/citations/18327081http://purl.uniprot.org/core/author"Maddedu P."xsd:string
http://purl.uniprot.org/citations/18327081http://purl.uniprot.org/core/date"2008"xsd:gYear
http://purl.uniprot.org/citations/18327081http://purl.uniprot.org/core/name"J Hypertens"xsd:string
http://purl.uniprot.org/citations/18327081http://purl.uniprot.org/core/pages"714-720"xsd:string
http://purl.uniprot.org/citations/18327081http://purl.uniprot.org/core/title"Genetic and dietary control of plasma tissue kallikrein secretion and urinary kinins exretion in man."xsd:string
http://purl.uniprot.org/citations/18327081http://purl.uniprot.org/core/volume"26"xsd:string
http://purl.uniprot.org/citations/18327081http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/18327081
http://purl.uniprot.org/citations/18327081http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/18327081
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