To examine the association between insertion/deletion (I/D) polymorphism of the angiotensin converting enzyme (ACE) gene and essential hypertension in a Chinese population, a case-control study was conducted using 157 hypertensive and 115 normotensive subjects. The I/D polymorphism of the ACE gene was identified by polymerase chain reaction. Plasma ACE activity was determined using spectrophotometry. The difference of allele frequencies between normotensives and hypertensives was statistically significant (chi 2 = 4.467, P = .035), while the genotype distribution was not different between normotensive and hypertensive subjects (chi 2 = 3.954, P = .138). Plasma ACE activity was highest in the DD genotype, followed by the ID genotype, and the lowest in the II genotype (P = .0001 in normotensives and P = .163 in hypertensives, respectively). Thus, we conclude that the ACE gene polymorphism is not associated with essential hypertension in this Chinese population, but plasma ACE activity is genetically determined in the normotensive Chinese.

Heart rate turbulence of turbulence onset and turbulence slope is critically vagal dependent and highly correlated with spontaneous baroreflex sensitivity, which underscores its clinical importance in cardiovascular risk stratification.

Both cDNA microarray and two-dimensional polyacrylamide protein electrophoresis studies revealed characteristic changes in AF tissue. We demonstrated the reprogramming of myosin regulatory light chain isoform composition, with a significant increase of its ventricular isoform (MLC-2V).

The molecular variant M235T, but not T174M, of the AGT gene is associated significantly with essential hypertension in this Taiwanese population. The genotype C/C or allele C is a risk factor for hypertension. The underlying mechanism of this association needs to be elucidated further.

1 The formation of advanced glycation endproducts (AGEs) on collagen within the arterial wall may be responsible for the development of diabetic vascular injury. This study was to examine the role of aminoguanidine (AG), an inhibitor of AGEs formation, in the prevention of arterial stiffening and cardiac hypertrophy in streptozotocin (STZ) induced diabetes in rats. 2 Diabetes was induced in animals by a single tail vein injection with 65 mg kg À1 STZ. After confirmation of the development of hyperglycemia (2 days later), rats were treated for 8 weeks with AG (daily peritoneal injections of 50 mg kg À1 ) and compared with the age-matched untreated diabetic controls.3 After exposure to AG, the STZ-diabetic rats showed no alterations in cardiac output, aortic pressure profiles, total peripheral resistance, and aortic characteristic impedance. 4 By contrast, treatment of this experimental diabetes with AG resulted in a significant increase in wave transit time (t), from 20.470.6 to 24.770.5 ms (Po0.05) and a decrease in wave reflection factor (R f ), from 0.7870.04 to 0.5370.02 (Po0.05). The decreased R f associated with the increased t suggest that AG may retard the diabetes-induced augmentation in systolic load of the left ventricle coupled to its arterial system. 5 Meanwhile, the diminished ratio of left ventricular weight to body weight suggests that prevention of the diabetes-related cardiac hypertrophy by AG may correspond to the drug-induced decline in aortic stiffening. 6 Glycation-derived modification on aortic collagen was also found to be enhanced in rats with diabetes ( þ 65.3%, Po0.05) and the advanced glycation process was retarded by AG treatment. 7 We conclude that long-term administration of AG to the STZ-treated rats imparts significant protection against the diabetes-derived deterioration in vascular dynamics, at least partly through inhibition of the AGEs accumulation on collagen in the arterial wall. Abbreviations: AG, aminoguanidine; AGEs, advanced glycation endproducts; BW, body weight (g); C, systemic arterial compliance (ml kg À1 mmHg À1 ); CO, cardiac output (ml kg À1 min À1 ); HR, basal heart rate (beats min À1 ); iNOS, inducible isoform of nitric oxide syntheses; LVW, left ventricular weight (g); NO, nitric oxide; P b , magnitude of the forward pressure (mmHg); P d , diastolic aortic pressure (mmHg); P f , magnitude of the forward pressure (mmHg); P m , mean aortic pressure (mmHg); P s , systolic aortic pressure (mmHg); R f , wave reflection factor; R p , total peripheral resistance (mmHg min kg ml À1 ); SDS-PAGE, sodium dodecyl sulfate-polyacrylamide gel electrophoresis; STZ, streptozotocin; SV, stroke volume (ml kg À1 beat À1 ); Z c , aortic characteristic impedance (mmHg min kg ml À1 ); Z i , aortic input impedance spectra (mmHg min kg ml À1 ); t, wave transit time (ms)