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ORIGINAL ARTICLE
Year : 2011  |  Volume : 1  |  Issue : 1  |  Page : 73-77

Effects of hydrochlorothiazide on K-dependent pancreatic response and the correlations with blood sugar, insulin in patients with essential hypertension


Molecular Science and Biomedical Unit and Department of Pharmacology, Faculty of Medicine, University of Ruhuna, Sri Lanka

Correspondence Address:
L M Hettihewa
Molecular Science and Biomedical Unit and Department of Pharmacology, Faculty of Medicine, University of Ruhuna
Sri Lanka
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2231-0738.77536

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Context: To study the onset of the development of glucose intolerance and the mechanism by hydrochlorothiazide (HCT). Settings and Design: Hypertensive patients (n = 120) who were treated with captopril (CP) 25 mg daily were randomly divided into two groups. Materials and Methods: The control group was on captopril (n = 60) and the test group was given 25 mg HCT. They were followed for six months and the levels of fasting blood sugar (FBS), fasting insulin (FI) , and fasting potassium (FK) were analyzed, to calculate the correlation coefficient. Results: There were no significant correlations between FBS and FI or FI, with FK in both groups at baseline. The changes in the FBS or FI levels during the first three months were not significant in both the test and control groups. Reduction of FK was significant (P < 0.05) and had a positive correlation with FBS after three months (r = + 0.78, P < 0.05) in the test group. Correlations between FI and FBS or FK were not significant. FBS was significantly increased (P < 0.05) in the test group after six months. Both FI and FK had developed significant correlations with FBS in the HCT-treated group (r = - 0.71 with FI and r = + 0.77 with FK, respectively, P < 0.05) after six months. Reduction of FI was positively correlated with the FK test group (r = + 0.83, P < 0.05) after six months. Conclusions: HCT induced hypokalaemia in the early phase and developed hyperglycemia and hyperinsulinemia in the late phase. This suggested that HCT initially influenced pancreatic response to glucose, which was dependent on serum K and was probably mediated by hypoinsulinemia. We suggest large scale studies for further investigations on this relationship.


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