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Titolo:
Interactive effect of PAI-1 4G/5G genotype and salt intake on PAI-1 antigen
Autore:
Brown, NJ; Murphey, LJ; Srikuma, N; Koschachuhanan, N; Williams, GH; Vaughan, DE;
Indirizzi:
Vanderbilt Univ, Med Ctr, Div Clin Pharmacol, Nashville, TN 37232 USA Vanderbilt Univ Nashville TN USA 37232 Pharmacol, Nashville, TN 37232 USA Vanderbilt Univ, Med Ctr, Div Cardiovasc Med, Nashville, TN 37232 USA Vanderbilt Univ Nashville TN USA 37232 ovasc Med, Nashville, TN 37232 USA Vet Adm Med Ctr, Nashville, TN USA Vet Adm Med Ctr Nashville TN USAVet Adm Med Ctr, Nashville, TN USA Harvard Univ, Sch Med, Div Endocrine Hypertens, Boston, MA USA Harvard Univ Boston MA USA Med, Div Endocrine Hypertens, Boston, MA USA Brigham & Womens Hosp, Boston, MA 02115 USA Brigham & Womens Hosp Boston MA USA 02115 mens Hosp, Boston, MA 02115 USA
Titolo Testata:
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
fascicolo: 6, volume: 21, anno: 2001,
pagine: 1071 - 1077
SICI:
1079-5642(200106)21:6<1071:IEOP4G>2.0.ZU;2-L
Fonte:
ISI
Lingua:
ENG
Soggetto:
PLASMINOGEN-ACTIVATOR INHIBITOR-1; CONVERTING ENZYME-INHIBITION; PLASMA FIBRINOLYTIC BALANCE; RENIN-ANGIOTENSIN SYSTEM; MYOCARDIAL-INFARCTION; IN-VIVO; ESSENTIAL-HYPERTENSION; CARDIOVASCULAR EVENTS; GENE-EXPRESSION; BLOOD-PRESSURE;
Keywords:
thrombosis; genetics; fibrinolysis; coagulation;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: Brown, NJ Vanderbilt Univ, Med Ctr, Div Clin Pharmacol, 560 RRB, Nashville, TN 37232USA Vanderbilt Univ 560 RRB Nashville TN USA 37232 ille, TN 37232USA
Citazione:
N.J. Brown et al., "Interactive effect of PAI-1 4G/5G genotype and salt intake on PAI-1 antigen", ART THROM V, 21(6), 2001, pp. 1071-1077

Abstract

Activation of the renin-angiotensin-aldosterone system (RAAS) is associated with increased circulating PAI-1 antigen and increased risk of thromboticcardiovascular events. A 4G/5G polymorphism located 675 bp upstream from the transcription start site of the PAI-I gene affects PAI-1 antigen concentrations. To test the hypothesis that PAI-I 4G/5G genotype influences the effect of activation of the RAAS on PAI-1 expression, we measured morning PAI-1 antigen concentrations in 76 subjects with essential hypertension duringlow (10 mmol/d) and high (200 mmol/d) salt intake. Low salt intake was associated with activation of the RAAS as measured by plasma renin activity (2.3 +/-0.2 versus 0.5 +/-0.0 ng angiotensin I-. mL(-1) h(-1), P <0.001) and aldosterone (529 +/- 40 versus 145 +/- 12 pmol/L). PAI-1 kantigen concentrations were 17.9 +/-2.7, 19.2 +/-2.5, and 27.8 +/-4.0 ng/mL during high saltintake and 19.2 +/-2.7, 21.6 +/-2.9, and 38.9 +/-7.2 ng/mL during low saltintake in the 5G/5G (n=14), 4G/5G (n=40), and 4G/4G (n=22) groups, respectively. There was a significant effect of both salt intake (F=6.0, P=0.017) and PAI-I 4G/5G genotype (F=7.6, P=0.001) on PAI-1 antigen. More importantly, there was a significant interactive effect (F= 7.8, P=0.001) of salt intake and PAI-I 4G/5G genotype on PAI-I antigen. PAI-1 4G/5G genotype influenced the relationship between serum triglycerides and PAI-1 antigen such that the relationship was significant only in 4G homozygotes during either high (R-2=0.31, P=0.014) or low (R-2=0.37, P=0.006) salt intake. This study identifies an important gene-by-environment interaction that may influence cardiovascular morbidity and the response to pharmacological therapies that interrupt the RAAS.

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Documento generato il 13/08/20 alle ore 14:54:53