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Blood pressure reduction due to hemoglobin glycosylation in type 2 diabetic patients
Pedro Cabrales1, Miguel A Salazar Vázquez, Beatrizy Salazar Vázquez
1La Jolla Bioengineering Institute, La Jolla, California, USA.
Insights
Glycosylation of hemoglobin (HbA1c) may lower blood pressure in type 2 diabetes patients not treated for hypertension. However, hypertension treatment might negate this effect, potentially due to endothelial dysfunction.
Area of Science:
- Endocrinology
- Cardiovascular Medicine
- Metabolic Disorders
Background:
- Glycosylation of hemoglobin (HbA1c) is a marker of glycemic control in diabetes.
- The relationship between HbA1c and hypertension risk is not fully understood.
- Endothelial function plays a crucial role in blood pressure regulation.
Purpose of the Study:
- To investigate whether hemoglobin glycosylation is a risk factor for hypertension.
- To explore the association between HbA1c levels and mean arterial pressure (MAP) in diabetic individuals.
- To examine the influence of hypertension treatment on the relationship between HbA1c and MAP.
Main Methods:
- Cross-sectional study of 129 diabetic subjects without specific comorbidities.
- Measurement of mean arterial pressure (MAP) and glycosylated hemoglobin (HbA1c).
- Analysis of the correlation between MAP and HbA1c, with and without adjustment for hypertension treatment.
Main Results:
- MAP was not directly correlated with HbA1c concentration when all patients were included.
- In untreated hypertensive patients, higher HbA1c levels were associated with lower MAP.
- In patients treated for hypertension, higher HbA1c levels were associated with higher MAP.
Conclusions:
- Hemoglobin glycosylation may exert an antihypertensive effect in type 2 diabetic patients not receiving hypertension treatment.
- Hypertension treatment in diabetic patients may be linked to endothelial dysfunction, potentially masking the blood pressure-lowering effect of HbA1c.
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.
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