Circadian blood pressure variation in normotensive type 2 diabetes patients and angiotensin converting enzyme polymorphism.
OBJECTIVE
Loss of circadian blood pressure (BP) variation (i.e., lack of nocturnal BP dip by at least 10mmHg, 'non-dipping') is associated with increased mortality rate in subjects with diabetes. We studied whether angiotensin converting enzyme (ACE) insertion/deletion (I/D) gene polymorphism may play a role in 24-h BP rhythm control.


METHODS
The study group was 38 normotensive normoalbuminuric type 2 diabetes patients with impaired BP variation, the controls were 51 well-matched type 2 diabetes subjects with normal 24-h BP rhythm. ACE I/D polymorphism, endothelial function and subclinical inflammation parameters (serum endothelin-1, sE-selectin, intercellular and vascular cell adhesion molecules, tumor necrosis factor-alpha) were assessed.


RESULTS
ACE DD genotype was found in 20 (53%), ID genotype in 16 (42%), and II genotype in 2 (5%) study group subjects, while 5 (10%) control subjects had DD genotype, 30 (59%) - ID genotype, and 16 (31%) - II genotype (p<0.0001). Study group subjects presented with marked endothelial dysfunction.


CONCLUSIONS
Impaired circadian blood pressure variation in normotensive normoalbuminuric type 2 diabetes patients is associated with ACE DD genotype and marked endothelial dysfunction when compared to diabetic subjects with normal blood pressure rhythm.
Czupryniak
Leszek
L
Department of Diabetology and Metabolic Diseases, Medical University of Lodz, Lodz, Poland. bigosik@poczta.onet.pl
Młynarski
Wojciech
W
Pawłowski
Maciej
M
Saryusz-Wolska
Małgorzata
M
Borkowska
Anna
A
Klich
Izabela
I
Bodalski
Jerzy
J
Loba
Jerzy
J
D000368:Aged; D001794:Blood Pressure; D002940:Circadian Rhythm; D003924:Diabetes Mellitus, Type 2 / Q000201:enzymology / Q000235:genetics* / Q000503:physiopathology*; D003971:Diastole; D019040:E-Selectin / Q000032:analysis; D004730:Endothelium, Vascular / Q000503:physiopathology; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D016254:Mutagenesis, Insertional; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D012016:Reference Values; D017384:Sequence Deletion; D013599:Systole; D019010:Vascular Cell Adhesion Molecule-1 / Q000032:analysis
D019040:E-Selectin; D019010:Vascular Cell Adhesion Molecule-1; D007703:Peptidyl-Dipeptidase A