title: Blood pressure reduction due to hemoglobin glycosylation in type 2 diabetic patients.
abstract: OBJECTIVE
  To test the hypothesis that glycosylation of hemoglobin constitutes a risk factor for hypertension.
  
  
  METHODS
  A total of 129 relative uniform diabetic subjects (86 women and 42 men) were enrolled in a cross-sectional study. Exclusion criteria included alcohol consumption, smoking, ischemic heart disease, stroke, neoplasia, renal, hepatic, and chronic inflammatory disease. Systolic and diastolic pressures were recorded in subsequent days and mean arterial blood pressure (MAP) was determined. Hemoglobin glycosylation was measured by determining the percentage glycosylated hemoglobin (HbAlc) by means of the automated microparticle enzyme immunoassay test.
  
  
  RESULTS
  MAP was found to be independent of the concentration of HbA1c; however, correcting MAP for the variability in hematocrit, to evidence the level of vasoconstriction (or vasodilatation) showed that MAP is negatively correlated with the concentration of HbA1c (p for trend <0.05), when patients treated for hypertension are excluded from the analysis. Patients treated for hypertension showed the opposite trend with increasing MAP as HbAlc increased (p for the difference in trends <0.05).
  
  
  CONCLUSIONS
  Glycosylation per se appears to lead to blood pressure reduction in type 2 diabetic patients untreated for hypertension. Treatment for hypertension may be associated with a level of endothelial dysfunction that interferes with the antihypertensive effect of HbA1c.
authors.affiliation: La Jolla Bioengineering Institute, La Jolla, California, USA.
authors.forename: Pedro
authors.initials: P
authors.lastname: Cabrales
authors.forename: Miguel A
authors.initials: MA
authors.lastname: Salazar Vázquez
authors.forename: Beatrizy
authors.initials: B
authors.lastname: Salazar Vázquez
authors.forename: Martha
authors.initials: M
authors.lastname: Rodríguez-Morán
authors.forename: Marcos
authors.initials: M
authors.lastname: Intaglietta
authors.forename: Fernando
authors.initials: F
authors.lastname: Guerrero-Romeros
mesh_terms: D000959:Antihypertensive Agents / Q000627:therapeutic use*; D001786:Blood Glucose / Q000187:drug effects; D001794:Blood Pressure / Q000187:drug effects*; D003430:Cross-Sectional Studies; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy / Q000378:metabolism* / Q000503:physiopathology; D005260:Female; D006442:Glycated Hemoglobin / Q000378:metabolism*; D006400:Hematocrit; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000378:metabolism* / Q000503:physiopathology; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged
chemical_list: D000959:Antihypertensive Agents; D001786:Blood Glucose; D006442:Glycated Hemoglobin; D007004:Hypoglycemic Agents; C517652:hemoglobin A1c protein, human