Open AccessDiuretic‐Induced Potassium Depletion and Glucose Intolerance Are Not Related to Hyperactivity of the Renin‐Angiotensin‐Aldosterone System in Hypertensive Patients With the Metabolic Syndrome
Author(s) -
Barbieri Douglas E.,
RibeiroFilho Fernando F.,
Ribeiro Artur B.,
Zanella Maria T.
Publication year - 2009
Publication title -
the journal of clinical hypertension
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 67
eISSN - 1751-7176
pISSN - 1524-6175
DOI - 10.1111/j.1751-7176.2009.00164.x
Subject(s) - medicine , endocrinology , aldosterone , plasma renin activity , diuretic , insulin resistance , homeostasis , renin–angiotensin system , insulin , blood pressure
The metabolic syndrome (MS) has been associated with hyperactivity of the renin‐angiotensin‐aldosterone system (RAAS). To assess the hypothesis that diuretic therapy in MS patients through further stimulation of RAAS would elicit greater potassium (K) depletion, two groups of hypertensive patients with (MS group [MSG]; n=20) and without (control group [CG]; n=19) MS were studied. Plasma renin activity (PRA), aldosterone (PA), and K levels were determined and an oral glucose tolerance test with plasma insulin determinations for calculation of homeostasis model assessment of insulin resistance (HOMA‐IR), sensitivity (ISI), and secretion (HOMA‐β) was performed, both before and 12 weeks after hydrochlorothiazide (HCT; 25 mg/d) therapy. At baseline, higher HOMA IR and HOMA‐β and lower ISI and plasma K were found in the MSG than in the CG, with no differences in PA and PRA between groups. 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‐β 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.