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Blood pressure reduction due to hemoglobin glycosylation in type 2 diabetic patients

Original Research

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Authors: Pedro Cabrales, Miguel A Salazar Vázquez, Beatriz Y Salazar Vázquez, Martha Rodríguez-Morán, Marcos Intaglietta, Fernando Guerrero-Romero

Published Date Volume 2008:4(4) Pages 917 - 922
DOI: http://dx.doi.org/10.2147/VHRM.S3077

Pedro Cabrales1, Miguel A Salazar Vázquez2,3, Beatriz Y Salazar Vázquez3,4, Martha Rodríguez-Morán5, Marcos Intaglietta4, Fernando Guerrero-Romero5

1La Jolla Bioengineering Institute, La Jolla, California, USA; 2Hospital Regional No. 1, of the Mexican Social Security Institute, Victoria de Durango, Dgo. Mexico; 3Faculty of Medicine and Dept. of Physical Chemistry, Universidad Juárez del Estado de Durango, Victoria de Durango, Dgo. Mexico; 4Department of Bioengineering, University of California, San Diego, La Jolla, California, USA; 5Biomedical Research Unit, of the Mexican Social Security Institute, Victoria de Durango, Dgo. Mexico

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 (HbA1c) 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 HbA1c 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.

Keywords: diabetes, hemoglobin glycosylation, hypertension, hematocrit, nitric oxide






 

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