OBJECTIVE: To explore the association of SDF1 3A genetic polymorphism with susceptibility of essential hypertension and captopril efficacy in patients with essential hypertension. METHODS: A total of 214 patients with essential hypertension and 228 healthy controls were genotyped for SDF1 3A polymorphism by polymerase chain reaction-restriction fragment length polymorphism assay. Among 39 subjects with different SDF1 3A of genotypes, 13 hypertensive patients simultaneously took oral captopril (25 mg/d) and nitrendipine (30 mg/d), and 12 patients orally received nitrendipine alone for 8 consecutive weeks, and 14 healthy controls did not take any agents. The blood pressure of all subjects was measured to evaluate the therapeutic efficacy. RESULTS: There was a significant difference in the plasma SDF-1 level in individuals with AA+AG genotypes or GG genotypes of SDF1 3A treated with nitrendipine plus captopril compared with healthy control (P < 0.05). Carriers with AA genotypes of SDF1 3A had lower total protein and globulin than those with GG genotypes (P < 0.05). After captopril treatment, hypertensive patients with AA+AG genotypes had bigger attenuated systolic blood pressure compared with those with GG genotypes (P < 0.05). CONCLUSION: Genetic polymorphism of SDF1 3A could influence the therapeutic efficacy of captopril in Chinese hypertensive patients.
OBJECTIVE: To explore the association of SDF1 3A genetic polymorphism with susceptibility of essential hypertension and captopril efficacy in patients with essential hypertension. METHODS: A total of 214 patients with essential hypertension and 228 healthy controls were genotyped for SDF1 3A polymorphism by polymerase chain reaction-restriction fragment length polymorphism assay. Among 39 subjects with different SDF1 3A of genotypes, 13 hypertensivepatients simultaneously took oral captopril (25 mg/d) and nitrendipine (30 mg/d), and 12 patients orally received nitrendipine alone for 8 consecutive weeks, and 14 healthy controls did not take any agents. The blood pressure of all subjects was measured to evaluate the therapeutic efficacy. RESULTS: There was a significant difference in the plasma SDF-1 level in individuals with AA+AG genotypes or GG genotypes of SDF1 3A treated with nitrendipine plus captopril compared with healthy control (P < 0.05). Carriers with AA genotypes of SDF1 3A had lower total protein and globulin than those with GG genotypes (P < 0.05). After captopril treatment, hypertensivepatients with AA+AG genotypes had bigger attenuated systolic blood pressure compared with those with GG genotypes (P < 0.05). CONCLUSION: Genetic polymorphism of SDF1 3A could influence the therapeutic efficacy of captopril in Chinese hypertensivepatients.