title: A preliminary study on T-786C endothelial nitric oxide synthase gene and renal hemodynamic and blood pressure responses to dietary sodium.
abstract: The purpose of the present study was to examine the role of the T-786C endothelial nitric oxide synthase (eNOS) gene polymorphism on changes in renal hemodynamics and blood pressure due to Na(+) loading. Twenty-eight older (63+/-1 years), moderately obese (39+/-2 % fat) hypertensives had their glomerular filtration rate (GFR), renal plasma flow (RPF), blood pressure (BP) and plasma nitric oxide (NO(x)) levels determined after eight days of low (20 mEq) and high (200 mEq) Na(+) diets. The two Na(+) diets were separated by a 1-week washout period. Subjects were genotyped for the eNOS-786 site and were grouped on whether they were homozygous or heterozygous for the C allele (TC+CC, n=13) or only homozygous for the T allele (TT, n=15). The TC+CC genotype group had a significantly greater increase in diastolic (P=0.021) and mean arterial (P=0.018) BP and a significant decline in both RPF (P=0.007) and GFR (P=0.029) compared to the TT genotype group with Na(+) loading. Furthermore, Na(+) loading resulted in a significant (P=0.036) increase in plasma NO(x) in the TT, but not in the TC+CC genotype group as well as a trend (P=0.051) for an increase in urine NO(x) in TC+CC, but not in the TT genotype group. The increase in BP during Na(+) loading in older hypertensives was associated with the eNOS genotype and may be related to changes in renal hemodynamics due to changes in NO metabolism.
authors.affiliation: University of Minnesota, Minneapolis, USA. denge001@umn.edu
authors.forename: D R
authors.initials: DR
authors.lastname: Dengel
authors.forename: M D
authors.initials: MD
authors.lastname: Brown
authors.forename: R E
authors.initials: RE
authors.lastname: Ferrell
authors.forename: T H
authors.initials: TH
authors.lastname: Reynolds
authors.forename: M A
authors.initials: MA
authors.lastname: Supiano
mesh_terms: D001794:Blood Pressure / Q000187:drug effects*; D004039:Diet, Sodium-Restricted; D004311:Double-Blind Method; D005260:Female; D020022:Genetic Predisposition to Disease; D005919:Glomerular Filtration Rate / Q000187:drug effects; D006579:Heterozygote; D006720:Homozygote; D006801:Humans; D006973:Hypertension / Q000201:enzymology / Q000235:genetics* / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D009569:Nitric Oxide / Q000097:blood; D052250:Nitric Oxide Synthase Type III / Q000235:genetics* / Q000378:metabolism; D010641:Phenotype; D010865:Pilot Projects; D011110:Polymorphism, Genetic; D012079:Renal Circulation / Q000187:drug effects*; D012720:Severity of Illness Index; D012964:Sodium / Q000097:blood / Q000652:urine; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage*; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D017673:Sodium Chloride, Dietary; D009569:Nitric Oxide; D012964:Sodium; C496314:NOS3 protein, human; D052250:Nitric Oxide Synthase Type III