المؤلفون: Johnson, T, Gaunt, TR, Newhouse, SJ, Padmanabhan, S, Tomaszewski, M, Kumari, M, Morris, RW, Tzoulaki, I, O'Brien, ET, Poulter, NR, Sever, P, Shields, DC, Thom, S, Wannamethee, SG, Whincup, PH, Brown, MJ, Connell, JM, Dobson, RJ, Howard, PJ, Mein, CA, Onipinla, A, Shaw-Hawkins, S, Zhang, Y, Smith, GD, Day, INM, Lawlor, DA, Goodall, AH, Fowkes, FG, Abecasis, GR, Elliott, P, Gateva, V, Braund, PS, Burton, PR, Nelson, CP, Tobin, MD, van der Harst, P, Glorioso, N, Neuvrith, H, Salvi, E, Staessen, JA, Stucchi, A, Devos, N, Jeunemaitre, X, Plouin, PF, Tichet, J, Juhanson, P, Org, E, Putku, M, Sober, S, Veldre, G, Viigimaa, M, Levinsson, A, Rosengren, A, Thelle, DS, Hastie, CE, Hedner, T, Lee, WK, Melander, O, Wahlstrand, B, Hardy, R, Wong, A, Cooper, JA, Palmen, J, Chen, L, Stewart, AFR, Wells, GA, Westra, HJ, Wolfs, MGM, Clarke, R, Franzosi, MG, Goel, A, Hamsten, A, Lathrop, M, Peden, JF, Seedorf, U, Watkins, H, Ouwehand, WH, Sambrook, J, Stephens, J, Casas, JP, Drenos, F, Holmes, MV, Kivimaki, M, Shah, S, Shah, T, Talmud, PJ, Whittaker, J, Wallace, C, Delles, C, Laan, M, Kuh, D, Humphries, SE, Nyberg, F, Cusi, D, Roberts, R, Newton-Cheh, C, Franke, L, Stanton, AV, Dominiczak, AF, Farrall, M, Hingorani, AD, Samani, NJ, Caulfield, MJ, Munroe, PB

المصدر: American journal of human genetics. 89(6):688-700

مصطلحات موضوعية: Medicin och hälsovetenskap

الوصول الحر: http://kipublications.ki.se/Default.aspx?queryparsed=id:123740960Test

المؤلفون: Padmanabhan, S, Melander, O, Johnson, T, Di Blasio, AM, Lee, WK, Gentilini, D, Hastie, CE, Menni, C, Monti, MC, Delles, C, Laing, S, Corso, B, Navis, G, Kwakernaak, AJ, van der Harst, P, Bochud, M, Maillard, M, Burnier, M, Hedner, T, Kjeldsen, S, Wahlstrand, B, Sjogren, M, Fava, C, Montagnana, M, Danese, E, Torffvit, O, Hedblad, B, Snieder, H, Connell, JMC, Brown, M, Samani, NJ, Farrall, M, Cesana, G, Mancia, G, Signorini, S, Grassi, G, Eyheramendy, S, Wichmann, HE, Laan, M, Strachan, DP, Sever, P, Shields, DC, Stanton, A, Vollenweider, P, Teumer, A, Volzke, H, Rettig, R, Newton-Cheh, C, Arora, P, Zhang, F, Soranzo, N, Spector, TD, Lucas, G, Kathiresan, S, Siscovick, DS, Luan, JA, Loos, RJF, Wareham, NJ, Penninx, BW, Nolte, IM, McBride, M, Miller, WH, Nicklin, SA, Baker, AH, Graham, D, McDonald, RA, Pell, JP, Sattar, N, Welsh, P, Munroe, P, Caulfield, MJ, Zanchetti, A, Dominiczak, AF, Global BPgen Consortium

مصطلحات موضوعية: TAMM-HORSFALL PROTEIN, CHRONIC KIDNEY-DISEASE, URINARY-EXCRETION, RISK-FACTORS, LOCI, NEPHROPATHY, FEASIBILITY, MUTATIONS, MORTALITY, BURDEN

الوصف: British Heart Foundation (BHF) Chair CH/98001 to AFD; BHF Programme RG/07/005/23633 to AFD, SP, CD; BHF Special Project Grant SP/08/005/25115 to AFD, SP, CD; SP was supported by an intermediate research fellowship from the BHF (FS/05/095/19937). We thank the British Heart Foundation, European Community Framework 6 Network of Excellence InGenious HyperCare, Fondazione Istituto Auxologico Italiano, and Regione Lombardia for funding the discovery study and validation in the MONICA/PAMELA populations. The discovery study and validations in the MONICA/ PAMELA populations are part of the activities of the EC Network of Excellence InGenious HyperCare (LSMH-CT-2006-037093) coordinated by Prof. A Zanchetti. Further financial support has been provided by Fondazione Istituto Auxologico Italiano, Milan, and Regione Lombardia

وصف الملف: ? - ?

العلاقة: PLOS GENET; e1001177; http://qmro.qmul.ac.uk/xmlui/handle/123456789/19180Test

الإتاحة: https://doi.org/10.1371/journal.pgen.1001177Test
http://qmro.qmul.ac.uk/xmlui/handle/123456789/19180Test

المؤلفون: Padmanabhan, S, Melander, O, Johnson, T, Di Blasio, A, Lee, W, Gentilini, D, Hastie, C, Menni, C, Monti, M, Delles, C, Laing, S, Corso, B, Navis, G, Kwakernaak, A, van der Harst, P, Bochud, M, Maillard, M, Burnier, M, Hedner, T, Kjeldsen, S, Wahlstrand, B, Sjogren, M, Fava, C, Montagnana, M, Danese, E, Torffvit, O, Hedblad, B, Snieder, H, Connell, J, Brown, M, Samani, N, Farrall, M, Cesana, G, Mancia, G, Signorini, S, Grassi, G, Eyheramendy, S, Wichmann, H, Laan, M, Strachan, D, Sever, P, Shields, D, Stanton, A, Vollenweider, P, Teumer, A, Volzke, H, Rettig, R, Newton-Cheh, C, Arora, P, Zhang, F, Soranzo, N, Spector, T, Lucas, G, Kathiresan, S, Siscovick, D, Luan, J, Loos, R, Wareham, N, Penninx, B, Nolte, I, McBride, M, Miller, W, Nicklin, SA, Baker, A, Graham, D, McDonald, R, Pell, J, Sattar, N, Welsh, P, Munroe, P, Caulfield, M, Zanchetti, A, Dominiczak, A

الوصف: Hypertension is a heritable and major contributor to the global burden of disease. The sum of rare and common genetic variants robustly identified so far explain only 1%-2% of the population variation in BP and hypertension. This suggests the existence of more undiscovered common variants. We conducted a genome-wide association study in 1,621 hypertensive cases and 1,699 controls and follow-up validation analyses in 19,845 cases and 16,541 controls using an extreme case-control design. We identified a locus on chromosome 16 in the 5andapos; region of Uromodulin (UMOD; rs13333226, combined P value of 3.6 x 1011). The minor G allele is associated with a lower risk of hypertension (OR [95%CI]: 0.87 [0.84-0.91]), reduced urinary uromodulin excretion, better renal function; and each copy of the G allele is associated with a 7.7% reduction in risk of CVD events after adjusting for age, sex, BMI, and smoking status (H.R.=0.923, 95% CI 0.860-0.991; p=0.027). In a subset of 13,446 individuals with estimated glomerular filtration rate (eGFR) measurements, we show that rs13333226 is independently associated with hypertension (unadjusted for eGFR: 0.89 [0.83-0.96], p=0.004; after eGFR adjustment: 0.89 [0.83-0.96], p=0.003). In clinical functional studies, we also consistently show the minor G allele is associated with lower urinary uromodulin excretion. The exclusive expression of uromodulin in the thick portion of the ascending limb of Henle suggests a putative role of this variant in hypertension through an effect on sodium homeostasis. The newly discovered UMOD locus for hypertension has the potential to give new insights into the role of uromodulin in BP regulation and to identify novel drugable targets for reducing cardiovascular risk.

العلاقة: https://ora.ox.ac.uk/objects/uuid:342c7f5d-2627-4c5f-82ec-55f3d503f6fdTest; https://doi.org/10.1371/journal.pgen.1001177Test

الإتاحة: https://doi.org/10.1371/journal.pgen.1001177Test
https://ora.ox.ac.uk/objects/uuid:342c7f5d-2627-4c5f-82ec-55f3d503f6fdTest

المؤلفون: Wahlstrand, B, Yakymenko, Iryna, Berggren, Karl-Fredrik

المصدر: Physical Review E. Statistical, Nonlinear, and Soft Matter Physics. 89(062910)

الوصف: A basic quantum-mechanical model for wave functions and current flow in open quantum dots or billiards is investigated. The model involves non-Hertmitian quantum mechanics, parity-time (PT) symmetry, and PT-symmetry breaking. Attached leads are represented by positive and negative imaginary potentials. Thus probability densities, currents flows, etc., for open quantum dots or billiards may be simulated in this way by solving the Schrödinger equation with a complex potential. Here we consider a nominally open ballistic quantum dot emulated by a planar microwave billiard. Results for probability distributions for densities, currents (Poynting vector), and stress tensor components are presented and compared with predictions based on Gaussian random wave theory. The results are also discussed in view of the corresponding measurements for the analogous microwave cavity. The model is of conceptual as well as of practical and educational interest.

وصف الملف: electronic

الوصول الحر: https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-107613Test
https://liu.diva-portal.org/smash/get/diva2:725849/FULLTEXT01.pdfTest

المؤلفون: Johnson, T., Newhouse, S. J., Howard, P. J., Onipinla, A., Shaw-Hawkins, S., Zhang, Y., Caulfield, M. J., Munroe, P. B., Gaunt, T. R., Smith, G. D., Day, I. N. M., Hamsten, A., Westra, H-J., Franke, L., Wolfs, M. G. M., Lawlor, D. A., Clarke, R., Franzosi, M. G., Goel, A., Peden, J. F., Watkins, H., Shah, T., Farrall, M., Lathrop, M., Seedorf, U., Ouwehand, W. H., Sambrook, J., Stephens, J., Tomaszewski, M., Casas, J-P., Whittaker, J., Kivimaki, M., Shah, S., Padmanabhan, S., Wallace, C., Nyberg, F., Goodall, A. H., Hastie, C. E., Lee, W. K., Delles, C., Dominiczak, A. F., Braund, P. S., Nelson, C. P., Samani, N. J., Burton, P. R., Salvi, E., Hingorani, A. D., Kumari, M., Holmes, M. V., Morris, R. W., Wannamethee, S. G., Tzoulaki, I., Abecasis, G. R., Elliott, P., O'Brien, E. T., Poulter, N. R., Cusi, D., Sever, P., Thom, S., Shields, D. C., Whincup, P. H., Brown, M. J., Connell, J. M., Gateva, V., Dobson, R. J., Mein, C. A., Newton-Cheh, C., Fowkes, F. G., Stanton, A. V., Tobin, M. D., Van Der Harst, P., Glorioso, N., Neuvrith, H., Talmud, P. J., Stucchi, A., Staessen, J. A., Devos, N., Jeunemaitre, X., Plouin, P-F., Viigimaa, M., Drenos, F., Tichet, J., Juhanson, P., Org, E., Putku, M., Sõber, S., Levinsson, A., Veldre, G., Laan, M., Rosengren, A., Thelle, D. S., Hedner, T., Wahlstrand, B., Melander, O., Hardy, R., Humphries, S. E., Wong, A., Kuh, D., Cooper, J. A., Palmen, J., Chen, L., Stewart, A. F. R., Wells, G. A., Roberts, R.

المصدر: Scopus ; http://www.scopus.com/home.urlTest

الوصف: Raised blood pressure (BP) is a major risk factor for cardiovascular disease. Previous studies have identified 47 distinct genetic variants robustly associated with BP, but collectively these explain only a few percent of the heritability for BP phenotypes. To find additional BP loci, we used a bespoke gene-centric array to genotype an independent discovery sample of 25,118 individuals that combined hypertensive case-control and general population samples. We followed up four SNPs associated with BP at our p < 8.56 × 10−7 study-specific significance threshold and six suggestively associated SNPs in a further 59,349 individuals. We identified and replicated a SNP at LSP1/TNNT3, a SNP at MTHFR-NPPB independent (r2 = 0.33) of previous reports, and replicated SNPs at AGT and ATP2B1 reported previously. An analysis of combined discovery and follow-up data identified SNPs significantly associated with BP at p < 8.56 × 10−7 at four further loci (NPR3, HFE, NOS3, and SOX6). The high number of discoveries made with modest genotyping effort can be attributed to using a large-scale yet targeted genotyping array and to the development of a weighting scheme that maximized power when meta-analyzing results from samples ascertained with extreme phenotypes, in combination with results from nonascertained or population samples. Chromatin immunoprecipitation and transcript expression data highlight potential gene regulatory mechanisms at the MTHFR and NOS3 loci. These results provide candidates for further study to help dissect mechanisms affecting BP and highlight the utility of studying SNPs and samples that are independent of those studied previously even when the sample size is smaller than that in previous studies. ; 103259

العلاقة: American Journal of Human Genetics, 2011, 89 (6), pp. 688-700; http://hdl.handle.net/2381/11590Test; http://www.sciencedirect.com/science/article/pii/S0002929711004472Test

الإتاحة: https://doi.org/10.1016/j.ajhg.2011.10.013Test
http://hdl.handle.net/2381/11590Test
http://www.sciencedirect.com/science/article/pii/S0002929711004472Test

المؤلفون: Padmanabhan, S., Melander, O., Johnson, T., Di Blasio, A. M., Lee, W. K., Gentilini, D., Hastie, C. E., Menni, C., Monti, M. C., Delles, C., Laing, S., Corso, B., Navis, G., Kwakernaak, A. J., van der Harst, P., Bochud, M., Maillard, M., Burnier, M., Hedner, T., Kjeldsen, S., Wahlstrand, B., Sjögren, M., Fava, C., Montagnana, M., Danese, E., Torffvit, O., Hedblad, B., Snieder, H., Connell, J. M., Brown, M., Samani, Nilesh J., Farrall, M., Cesana, G., Mancia, G., Signorini, S., Grassi, G., Eyheramendy, S., Wichmann, H. E., Laan, M., Strachan, D. P., Sever, P., Shields, D. C., Stanton, A., Vollenweider, P., Teumer, A., Völzke, H., Rettig, R., Newton-Cheh, C., Arora, P., Zhang, F., Soranzo, N., Spector, T. D., Lucas, G., Kathiresan, S., Siscovick, D. S., Luan, J., Loos, R. J., Wareham, N. J., Penninx, B. W., Nolte, I. M., McBride, M., Miller, W. H., Nicklin, S. A., Baker, A. H., Graham, D., McDonald, R. A., Pell, J. P., Sattar, N., Welsh, P., Global BPgen Consortium, Munroe, P., Caulfield, M. J., Zanchetti, A., Dominiczak, A. F.

المصدر: PubMed ; http://www.ncbi.nlm.nih.gov/pubmedTest/

مصطلحات موضوعية: Aged, Alleles, Blood Pressure, Chromosomes, Human, Pair 16, Female, Gene Frequency, Genetic Predisposition to Disease, Genome-Wide Association Study, Genotype, Glomerular Filtration Rate, Humans, Hypertension, Linear Models, Male, Meta-Analysis as Topic, Middle Aged, Multivariate Analysis, Polymorphism, Single Nucleotide, Proportional Hazards Models, Risk Factors, Survival Analysis, Uromodulin

الوصف: Hypertension is a heritable and major contributor to the global burden of disease. The sum of rare and common genetic variants robustly identified so far explain only 1%-2% of the population variation in BP and hypertension. This suggests the existence of more undiscovered common variants. We conducted a genome-wide association study in 1,621 hypertensive cases and 1,699 controls and follow-up validation analyses in 19,845 cases and 16,541 controls using an extreme case-control design. We identified a locus on chromosome 16 in the 5' region of Uromodulin (UMOD; rs13333226, combined P value of 3.6 × 10⁻¹¹). The minor G allele is associated with a lower risk of hypertension (OR [95%CI]: 0.87 [0.84-0.91]), reduced urinary uromodulin excretion, better renal function; and each copy of the G allele is associated with a 7.7% reduction in risk of CVD events after adjusting for age, sex, BMI, and smoking status (H.R. = 0.923, 95% CI 0.860-0.991; p = 0.027). In a subset of 13,446 individuals with estimated glomerular filtration rate (eGFR) measurements, we show that rs13333226 is independently associated with hypertension (unadjusted for eGFR: 0.89 [0.83-0.96], p = 0.004; after eGFR adjustment: 0.89 [0.83-0.96], p = 0.003). In clinical functional studies, we also consistently show the minor G allele is associated with lower urinary uromodulin excretion. The exclusive expression of uromodulin in the thick portion of the ascending limb of Henle suggests a putative role of this variant in hypertension through an effect on sodium homeostasis. The newly discovered UMOD locus for hypertension has the potential to give new insights into the role of uromodulin in BP regulation and to identify novel drugable targets for reducing cardiovascular risk. ; This research was supported by the following grants: British Heart Foundation (BHF) Chair CH/98001 to AFD; BHF Programme RG/07/005/23633 to AFD, SP, CD; BHF Special Project Grant SP/08/005/25115 to AFD, SP, CD; SP was supported by an intermediate research fellowship from the BHF ...

العلاقة: PLoS Genetics, 2010, 6 (10), pp. e1001177-e1001177; http://hdl.handle.net/2381/17270Test; http://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1001177Test

الإتاحة: https://doi.org/10.1371/journal.pgen.1001177Test
http://hdl.handle.net/2381/17270Test
http://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1001177Test

المؤلفون: Padmanabhan, S., Melander, O., Johnson, T., Di Blasio, A.M., Lee, W.K., Gentilini, D., Hastie, C.E., Menni, C., Monti, M.C., Delles, C., Laing, S., Corso, B., Navis, G., Kwakernaak, A.J., van der Harst, P., Bochud, M., Maillard, M., Burnier, M., Hedner, T., Kjeldsen, S., Wahlstrand, B., Sjogren, M., Fava, C., Montagnana, M., Danese, E., Torffvit, O., Hedblad, B., Snieder, H., Connell, J.M.C., Brown, M., Samani, N.J., Farrall, M., Cesana, G., Mancia, G., Signorini, S., Grassi, G., Eyheramendy, S., Wichmann, H.E., Laan, M., Strachan, D.P., Sever, P., Shields, D.C., Stanton, A., Vollenweider, P., Teumer, A., Volzke, H., Rettig, R., Newton-Cheh, C., Arora, P., Zhang, F., Soranzo, N., Spector, T.D., Lucas, G., Kathiresan, S., Siscovick, D.S., Luan, J.A., Loos, R.J.F., Wareham, N.J., Penninx, B.W.J.H., Nolte, I.M., McBride, M., Miller, W.H., Nicklin, S.A., Baker, A.H., Graham, D., McDonald, R.A., Pell, J.P., Sattar, N., Welsh, P., Munroe, P., Caulfield, M.J., Zanchetti, A., Dominiczak, A.F.

المصدر: Padmanabhan , S , Melander , O , Johnson , T , Di Blasio , A M , Lee , W K , Gentilini , D , Hastie , C E , Menni , C , Monti , M C , Delles , C , Laing , S , Corso , B , Navis , G , Kwakernaak , A J , van der Harst , P , Bochud , M , Maillard , M , Burnier , M , Hedner , T , Kjeldsen , S , Wahlstrand , B , Sjogren , M , Fava , C ....

وصف الملف: application/pdf

العلاقة: https://research.vumc.nl/en/publications/36d74cd9-ca33-4965-957d-c4891d01efbbTest

الإتاحة: https://doi.org/10.1371/journal.pgen.1001177Test
https://research.vumc.nl/en/publications/36d74cd9-ca33-4965-957d-c4891d01efbbTest
https://research.vumc.nl/ws/files/714466/257156.pdfTest

المؤلفون: Alvarez-Madrazo, S, Mackenzie, S, Davies, E, Fraser, R, Lee, W, Brown, M, Caulfield, M, Dominiczak, A, Farrall, M, Lathrop, M, Hedner, T, Melander, O, Munroe, P, Samani, N, Stewart, P, Wahlstrand, B, Webster, J, Palmer, C, Padmanabhan, S, Connell, J

الوصف: The locus encompassing the corticosteroidogenic genes CYP11B2 and CYP11B1 is of potential importance in essential hypertension. We analyzed the association of polymorphisms at this locus with risk of essential hypertension, using 2 white case-control collections for discovery (n=3340) and confirmation (n=2929). Single-marker and haplotype analyses were performed, with the CYP11B2 Intron 2 Conversion polymorphism showing strongest association with hypertension in both cohorts and in combined analysis (odds ratio=1.16, P=8.54×10(-5)). The CYP11B1 ACA haplotype associated with increased risk of hypertension relative to the alternative, GTC (odds ratio=1.11; P=7.4×10(-3)), whereas the CYP11B2 TWtC haplotype seemed protective relative to the contrasting CConvT (odds ratio=0.88, P=2.2×10(-3)). Analysis spanning the whole CYP11B1/CYP11B2 locus showed that haplotypes associated with raised risk of hypertension tend to coexist. Functional analysis of heterozygous human adrenal tissue demonstrated decreased CYP11B2 expression and increased CYP11B1 expression for those alleles associating with reduced risk of hypertension. These results confirm the hypertensive influence of this locus, with data suggesting a complex digenic mechanism whereby altered relative CYP11B1 and CYP11B2 gene expression could have a chronic effect on enzyme activity and corticosteroid synthesis.

العلاقة: https://ora.ox.ac.uk/objects/uuid:7c8d25a5-9e46-4abf-b630-5e0603d56aa3Test; https://doi.org/10.1161/hypertensionaha.112.200741Test

الإتاحة: https://doi.org/10.1161/hypertensionaha.112.200741Test
https://ora.ox.ac.uk/objects/uuid:7c8d25a5-9e46-4abf-b630-5e0603d56aa3Test

المؤلفون: TURNER ST, BOERWINKLE E, O'CONNELL JR, BAILEY KR, GONG Y, CHAPMAN AB, MCDONOUGH CW, BEITELSHEES AL, SCHWARTZ GL, GUMS JG, PADMANABHAN S, HILTUNEN TP, CITTERIO L, DONNER KM, HEDNER T, LANZANI C, MELANDER O, SAARELA J, RIPATTI S, WAHLSTRAND B, KONTULA K, DOMINICZAK AF, COOPER DEHOFF RM, JOHNSON J.A., MANUNTA , PAOLO

المساهمون: Turner, St, Boerwinkle, E, O'Connell, Jr, Bailey, Kr, Gong, Y, Chapman, Ab, Mcdonough, Cw, Beitelshees, Al, Schwartz, Gl, Gums, Jg, Padmanabhan, S, Hiltunen, Tp, Citterio, L, Donner, Km, Hedner, T, Lanzani, C, Melander, O, Saarela, J, Ripatti, S, Wahlstrand, B, Manunta, Paolo, Kontula, K, Dominiczak, Af, COOPER DEHOFF, Rm, Johnson, J. A.

العلاقة: info:eu-repo/semantics/altIdentifier/wos/WOS:000321962300031; volume:62; issue:2; firstpage:391; lastpage:397; numberofpages:7; journal:HYPERTENSION; http://hdl.handle.net/20.500.11768/12514Test; info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-84880932080

الإتاحة: https://doi.org/20.500.11768/12514Test
https://hdl.handle.net/20.500.11768/12514Test

المؤلفون: Svensson Färbom, P., Wahlstrand, B., Almgren, P., Dahlberg, J., Kjeldsen, S., Hedner, T., Melander, O., FAVA, Cristiano

المساهمون: Svensson Färbom, P., Wahlstrand, B., Almgren, P., Dahlberg, J., Fava, Cristiano, Kjeldsen, S., Hedner, T., Melander, O.

مصطلحات موضوعية: cardiovascular disease, hypertension, pharmacogenetics

الوصف: OBJECTIVE: The capability of the protein NEDD4L to reduce renal tubular expression of epithelial Na+ channel (ENaC) is influenced by a functional rs4149601 G→A NEDD4L polymorphism. As diuretics and β-blockers inhibit renal sodium reabsorption and renin release, respectively, we hypothesized that the β-blocker or diuretic-induced blood pressure reduction and prevention of cardiovascular disease would be greater in patients with the highest ENaC expression (rs4149601 G-allele), whereas there would be no such genetically mediated differences in treatment efficacy among patients treated with the vasodilator diltiazem.METHODS: We related rs4149601 status to 6-month blood pressure reduction and risk of cardiovascular events in 5152 hypertensive patients (DBP ≥ 100 mmHg) from the Nordic Diltiazem Study (NORDIL) randomized to either β-blocker and/or diuretic-based treatment or diltiazem-based treatment.RESULTS: In patients on β-blocker or diuretic monotherapy, carriers of the G-allele had greater SBP reduction (19.5 ± 16.8 vs. 15.0 ± 19.3 mmHg, P < 0.001) and DBP reduction (15.4 ± 8.3vs. 14.1 ± 8.4 mmHg, P = 0.02) and during 4.5 years of follow-up among patients randomized to β-blockers and/or diuretics, carriers of the G-allele had greater protection from cardiovascular events [relative risk (RR) = 0.52, 95% confidence interval (CI) = 0.36-0.74, P < 0.001] as compared to AA homozygotes. Within the diltiazem group, there was no difference in blood pressure reduction or risk of cardiovascular events according to genotype.CONCLUSION: The functional NEDD4L rs4149601 polymorphism influences the efficacy of β-blocker and/or diuretic-based antihypertensive treatment both in terms of blood pressure reduction and cardiovascular disease protection, whereas diltiazem-based antihypertensive treatment efficacy is not influenced by this NEDD4L polymorphism.

وصف الملف: STAMPA

العلاقة: info:eu-repo/semantics/altIdentifier/pmid/21052022; info:eu-repo/semantics/altIdentifier/wos/WOS:000285744600030; volume:29; issue:2; firstpage:388; lastpage:395; numberofpages:8; journal:JOURNAL OF HYPERTENSION; http://hdl.handle.net/11562/346179Test; info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-78651273887

الإتاحة: http://hdl.handle.net/11562/346179Test