RESUMO
OBJECTIVE: To examine whether there is an association essential hypertension pressure and a polymorphic Hind III biallelic marker in the non-recombining region of Y chromosome in Chinese Han people. METHODS: Peripheral blood samples were collected from 402 males with essential hypertension pressure and 455 age- and body height-matched healthy males as control group. Genomic DNA was extracted from the white blood cells. Segments of polymorphic Hind III restriction site of the Y chromosome were amplified from the genomic DNA by polymerase chain reaction (PCR). The PCR products were restricted with 10 U of Hind III overnight at 37 degrees C. The digested products were subjected to electrophoresis in 3% agarose gels, and stained with ethidium bromide. RESULTS: The Hind III (+) genotype was found in 58.5% of the men with essential hypertension (235/402), significantly lower than that in the healthy men (64.4%, 302/455, P = 0.02). The systolic blood pressure of the men with Hind III (+) genotype was 133.8 mm Hg +/- 25.2 mm Hg, significantly lower than that of the Hind III (-) genotype (138.0 mm Hg +/- 27.0 mm Hg, P < 0.05), and the diastolic blood pressure (DBP) of the men with Hind III (+) genotype was 83.5 mm Hg +/- 13.3 mm Hg, significantly lower than that of the men with Hind III (-) genotype (85.9 mm Hg +/- 14.4 mm Hg, P = 0.01), and the mean arterial pressure of the men with Hind III (+) genotype was 100.2 mm Hg +/- 16.5 mm Hg, significantly lower than that of the of the men with Hind III (+) genotype was (103.3 mm Hg +/- 17.6 mm Hg, P = 0.01). CONCLUSION: Polymorphic Hind III restriction site of the Y chromosome is associated with essential hypertension in Chinese Han people.
Assuntos
Cromossomos Humanos Y/genética , Desoxirribonuclease HindIII/genética , Hipertensão/genética , Estudos de Casos e Controles , China/epidemiologia , Humanos , Hipertensão/epidemiologia , Masculino , Pessoa de Meia-Idade , Polimorfismo de Fragmento de RestriçãoRESUMO
OBJECTIVE: Levels of adrenomedullin (AM), a potent vasodilatory peptide, have been shown to increase in the early stage of acute myocardial infarction (AMI). The purpose of this study was to determine whether coronary sinus-aortic step-up of mature forms of AM is accelerated in patients with AMI after reperfusion. METHODS: The subjects were 146 consecutive patients with a first episode of anterior AMI and 51 normal controls. All patients with AMI underwent balloon reperfusion therapy within 24 h after symptom onset. Plasma levels of two molecular forms of AM (an active, mature form [AM-m] and an intermediate, inactive glycine-extended form [AM-Gly]) in the aorta and coronary sinus (CS) were measured by specific immunoradiometric assay after reperfusion. RESULTS: Plasma levels of AM-m and AM-Gly in the aorta and CS were higher in AMI patients than in controls. CS-aortic step-up of AM-m, which is an index of myocardial production of AM-m, was significantly greater in AMI patients than in controls [(1.7 +/- 1.4) pmol/L vs (0.4 +/- 0.3) pmol/L, P < 0.01]. However, there was no significant difference in CS-aortic step-up of AM-Gly (P = 0.30). AMI patients with left ventricular dysfunction (n = 49) had a significantly higher CS-aortic AM-m step-up than AMI patients without left ventricular dysfunction (n = 97). AMm in the aorta and CS negatively correlated with the left ventricular ejection fraction (r = -0.50, r = -0.48, P < 0.01). CONCLUSION: Myocardial synthesis of AM-m is accelerated in patients with reperfused AMI, especially in patients with critical left ventricular dysfunction. Increased myocardial synthesis of active AM may protect against cardiac dysfunction, myocardial remodeling, or both after the onset of AMI.