In protocol 2, ACE genotypes as well as microalbuminuria and renal hemodynamic parameters were investigated in 75 patients with EH with normal renal function and a strong family history of hypertension.
The purpose of the current study is to investigate the association of I/D polymorphism of the ACE gene with essential hypertension in northern Indians.
These findings suggest that the effect of blood pressure on LVMI in essential hypertension is expressed only in the presence of the ACE gene deletion allele.
We investigated if renin-angiotensinaldosterone system associated genotypes (angiotensinogen [M235T] and ACE [I/D]) are related to blood pressure (BP), renal haemodynamics and sodium excretion in sex and age-matched (1835 years) healthy Caucasian offspring of either two parents with EH (n=101, EH-offspring) or two normotensive parents (n=50, controls).
After 6 weeks, the results showed that the ACE I/D polymorphism, not the CYP11B2 -344T/C polymorphism, was associated with systolic blood pressure (SBP) response to HCTZ (P = 0.009) in the Han Chinese population with essential hypertension, with no interaction.
These findings indicate that there is no association between the ACE gene and left ventricular hypertrophy in essential hypertension occurring in the Chinese population.
We found no evidence for linkage between essential hypertension and the genes coding for renin, angiotensinogen, angiotensin-converting enzyme, or kallikrein 1 in the 329 hypertensive individuals of 142 families studied.
The aim of the present study was to investigate the association of the angiotensin-converting enzyme2350 G/A polymorphism with atrial fibrillation in Han Chinese patients with essential hypertension.
The ACE (I/D) polymorphism showed no association with CHD, whereas the frequency distribution of AGT (M235T) genotypes among patients and controls (235T: 29.1% and 19.0%; M235T: 48.5% and 50.2%; M235: 22.4% and 30.8%, respectively) was statistically different (p = 0.005) and not related to the presence of essential hypertension.
Relationship between the angiotensin converting enzyme gene polymorphism and the effects of enalapril on left ventricular hypertrophy and impaired diastolic filling in essential hypertension: M-mode and pulsed Doppler echocardiographic studies.
To evaluate the potential implications of the genetic variability of angiotensin converting enzyme, angiotensinogen and angiotensin II type 1 receptor gene for essential hypertension in Tibetan.
Taken together, our data do not support the existence of a sex-specific association between the ACE I/D polymorphism and essential hypertension in the Japanese population.
The up-regulation in relative expression of circulating Angiotensin converting enzyme mRNA and protein in patients with respect to controls might be correlated with high blood pressure in patients with essential hypertension.
These results suggest that the ACE gene was not directly responsible for essential hypertension in this particular Japanese population with the same socioeconomic background.
Among females, ACE I/D and ACE2 rs2106809 polymorphisms, while among males, ACE2 rs2106809 polymorphism and alcohol consumption are associated with essential hypertension in the study population.
In conclusion, the polymorphisms in the GNB3 gene and ACE gene, solely or combined, did not confer a significantly increased risk for the development of EH in the Kazakh isolate of northeast China.
In addition to the angiotensin-converting enzyme (ACE) and angiotensinogen (AGT) gene variants, gene-gene interactions may be important causative factors in a complex disease such as young-onset essential hypertension.
The response of blood pressure and plasma renin activity (PRA) 1 h after 50 mg captopril administration were evaluated in 82 inpatients with untreated essential hypertension (42 men, 40 women; mean age +/- SD: 52 +/- 13 years; range: 27 to 79 years) in relation to ACE genotypes.
In addition, serum ACE2 (183.57 pg/ml; vs. 151.78 pg/ml; p = 0.02) and chymase (68.5 pg/ml; vs. 23.66 pg/ml; p = 0.034) were significantly higher in patients with uncontrolled EH than controlled EH in response to ACE-inhibitory therapy.