CONTRIBUTION OF ANGIOTENSIN-I-CONVERTING-ENZYME GENE POLYMORPHISM ANDANGIOTENSINOGEN GENE POLYMORPHISM TO BLOOD-PRESSURE REGULATION IN ESSENTIAL-HYPERTENSION

The renin-angiotensin system (RAS) is involved in the pathogenesis of essential hypertension. In the present study we examined the genotype frequencies of the insertion/deletion polymorphisms of the ACE gene an d the M235T polymorphism of the Angiotensinogen (Agt) gene in patients with essential hypertension in comparison with normotensive subjects. In hypertensive patients functional effects of blood pressure respons e to ACE inhibition were investigated. A total of 121 patients with es sential hypertension (group 1) and 125 normotensive control subjects ( group 2) were included in this study. All patients were genotyped by p olymerase chain reactions (PCR) for the insertion/deletion (I/D) polym orphism of the ACE gene and the M235T polymorphism of the Agt gene. To analyze possible functional impacts on blood pressure regulation 50 m g of captopril was administered to hypertensive patients. No significa nt association of essential hypertension with polymorphisms of the Agt and ACE gene was found. The ACE serum levels in patients with the DD- genotype of the ACE I/D polymorphism were higher than in patients with the II-genotype (P < .01). In patients with the ID-genotype the ACE s erum levels were in-between. A captopril test was performed in hyperte nsive patients. The patients were further divided into subgroups accor ding to the diastolic and systolic blood pressure response. Group la c onsisted of patients with a diastolic blood pressure drop of >5 mm Hg and group Ib with less than or equal to 5 mm Hg. Group Ic consisted of patients with a systolic blood pressure drop of >10 mm Hg and group 1 d with less than or equal to 10 mm Hg. Twice as many patients with the DD genotype of the ACE gene were found in group la compared to group Ib (chi(2) = 5.673; P = .017). No association of systolic blood pressu re change to the investigated polymorphisms was found. Our results do not support the hypothesis that the investigated polymorphisms contrib ute to essential hypertension. Furthermore, no major impact of these p olymorphisms on blood pressure response to captopril were detected. We conclude that the investigated genotypes have no influence on blood p ressure level and homeostasis. (C) 1998 American Journal of Hypertensi on, Ltd.