Linked Life Data

16172412

Source:http://linkedlifedata.com/resource/pubmed/id/16172412

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2005-9-30
pubmed:abstractText
Single nucleotide polymorphisms (SNPs) in genes encoding or influencing renal sodium transport systems were investigated as potential predictors of blood pressure (BP) response to a thiazide diuretic. A sample of 585 adults with essential hypertension (30 to 59.9 years of age; 50% blacks; 47% women) were treated with hydrochlorothiazide for 4 weeks (25 mg daily, orally) to determine office BP responses. Ambulatory BP responses were measured in a subset of 228 subjects. After adjustment for ethnicity, sex, age, and waist-to-hip ratio, 3 SNPs in WNK1 (rs2107614, rs2277869, and rs1159744), encoding a lysine-deficient protein kinase that regulates thiazide-sensitive sodium-potassium cotransport, made statistically significant contributions to predicting ambulatory BP responses, accounting for 2% to 4% of variation in systolic and diastolic responses (P<0.05). SNPs in the beta2-adrenoceptor (rs2400707) and the epithelial sodium channel gamma-subunit (rs5723 and rs5729) were associated with similar magnitude of variation in ambulatory systolic BP response (P=0.028) or office diastolic BP response (P<0.05), respectively. However, SNPs evaluated in the furosemide-sensitive sodium-potassium chloride cotransporter, potassium inwardly rectifying channel, chloride channel, thiazide-sensitive sodium chloride cotransporter, epithelial sodium channel beta-subunit, and the mineralocorticoid receptor were not associated with significant variation in ambulatory or office BP responses. Polymorphisms in genes regulating renal sodium transport, in particular WNK1, predict interindividual differences in antihypertensive responses to hydrochlorothiazide.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1524-4563
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
46
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
758-65
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:16172412-Adult, pubmed-meshheading:16172412-Biological Transport, pubmed-meshheading:16172412-Blood Pressure, pubmed-meshheading:16172412-Blood Pressure Monitoring, Ambulatory, pubmed-meshheading:16172412-Diastole, pubmed-meshheading:16172412-Epithelial Sodium Channel, pubmed-meshheading:16172412-Female, pubmed-meshheading:16172412-Humans, pubmed-meshheading:16172412-Hydrochlorothiazide, pubmed-meshheading:16172412-Hypertension, pubmed-meshheading:16172412-Intracellular Signaling Peptides and Proteins, pubmed-meshheading:16172412-Kidney, pubmed-meshheading:16172412-Male, pubmed-meshheading:16172412-Middle Aged, pubmed-meshheading:16172412-Polymorphism, Single Nucleotide, pubmed-meshheading:16172412-Protein-Serine-Threonine Kinases, pubmed-meshheading:16172412-Receptors, Adrenergic, beta-2, pubmed-meshheading:16172412-Sodium, pubmed-meshheading:16172412-Sodium Channels, pubmed-meshheading:16172412-Sodium Chloride Symporter Inhibitors, pubmed-meshheading:16172412-Systole
pubmed:year
2005
pubmed:articleTitle
WNK1 kinase polymorphism and blood pressure response to a thiazide diuretic.
pubmed:affiliation
Division of Nephrology and Hypertension, Department of Internal Medicine, Mayo Clinic and Foundation, Rochester, MN, USA. turner.stephen@mayo.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural