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Diuretic-Induced Potassium Depletion and Glucose Intolerance Are Not Related to Hyperactivity of the Renin-Angiotensin-Aldosterone System in Hypertensive Patients With the Metabolic Syndrome
The Journal of Clinical Hypertension, 09/15/09
Barbieri DE et al. – With therapy, PRA increased similarly in both groups while PA increased only in the MSG. However, greater reduction in plasma K occurred in the CG, and the 2 groups reached similar final K values. Impairment in glucose tolerance occurred in both groups, with no change in HOMA–beta in the CG and reduction in the MSG, suggesting that diuretic therapy increases insulin resistance and impairs insulin secretion independent of abdominal obesity. These alterations could not be attributed to hyperactivity of RAAS.
Douglas E. Barbieri, 09/15/09
| In contrast to other studies, our results did not show evidence of hyperactivity of RAAS in patients with abdominal obesity and metabolic syndrome. In a previous study, our group also observed that plasma potassium levels in abdominal obese patients, even without diuretic therapy, were lower than in nonobese hypertensive patients. This was attributed to a potential hyperactivity of the RAAS, not confirmed in the present study. Thus, the reasons for the lower levels of plasma K in our abdominal obese patients are not clear. The significant negative correlation found between baseline plasma insulin and plasma K in the present study could also suggest a role of hyperinsulinemia in the reduction of plasma potassium levels in abdominal obesity. Although more pronounced in obese patients, the disturbances in glucose metabolism induced by thiazide diuretic therapy seem independent of the presence of MS and can be attributed to worsening in both insulin resistance and secretion. |
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