RT Journal Article SR Electronic T1 Pharmacogenetic Implications of eNOS Polymorphisms (Glu298Asp, T786C, 4b/4a) in Cardiovascular Drug Therapy JF In Vivo JO In Vivo FD International Institute of Anticancer Research SP 1051 OP 1058 DO 10.21873/invivo.11573 VO 33 IS 4 A1 ANGELA COZMA A1 ADRIANA FODOR A1 OLGA HILDA ORASAN A1 ROMANA VULTURAR A1 DOREL SAMPLELEAN A1 VASILE NEGREAN A1 CRINA MURESAN A1 RAMONA SUHAROSCHI A1 ADELA SITAR-TAUT YR 2019 UL http://iv.iiarjournals.org/content/33/4/1051.abstract AB Endothelial nitric oxide synthase (NOS3 or eNOS) is the enzyme responsible for the highest production of nitric oxide, with the greatest impact on the cardiovascular system, encoded by the eNOS gene, which presents various polymorphisms. ENOS gene polymorphisms play an important role in the response to drugs affecting nitric oxide (NO) signaling. This review discusses the pharmacogenetic impact of eNOS polymorphisms on the response to drugs affecting NO activity: angiotensin converting enzyme inhibitors, angiotensin II receptor antagonists, calcium blockers, beta-blockers, diuretics, phosphodiesterase inhibitors, and statins. The identification of biomarkers that accurately predict particular phenotypes is a challenge that needs additional large studies, in different populations. Efforts should be oriented towards a more accurate evaluation of the effects of eNOS genetic variants on biochemical parameters reflecting eNOS gene expression and enzymatic activity, in different diseases, as well as following drug treatment. This approach will allow for a better understanding of the role of eNOS genetic variants in cardiovascular disease progression and for cardiovascular drug therapy optimization.