Improvement of insulin resistance by troglitazone ameliorates cardiac sympathetic nervous dysfunction in patients with essential hypertension.

Abstract

It was recently suggested that insulin resistance is significantly correlated with activation of the cardiac sympathetic nervous system in patients with essential hypertension. To examine the effects of troglitazone, an agent used to treat insulin resistance, on cardiac sympathetic nervous dysfunction and insulin resistance in patients with essential hypertension. The study participants included 34 patients (14 men, 20 women) with mild essential hypertension and 17 normal controls (group C, seven men). The patients were randomly divided into two groups, one treated with 400 mg troglitazone and antihypertensive drugs (group T, n = 17) and the other treated with antihypertensive drugs only (group N, n = 17). We evaluated insulin resistance and cardiac sympathetic nervous function before and after 6 months of treatment. Insulin resistance was evaluated using steady-state plasma glucose (SSPG; mg/dl) concentrations and cardiac sympathetic nervous function was evaluated using the heart-to-mediastinum ratio (H : M) and mean washout rate measured by 123I-meta-iodobenzylguanidine (MIBG) cardiac imaging. There were significant differences in SSPG (P < 0.01), early (P < 0.05) and delayed (P < 0.05) phases of H : M and washout rate (P < 0.05) between the hypertensive patients and group C. The SSPG concentration was significantly improved after treatment only in group T, from 153.3 to 123.7 mg/dl (P < 0.01). The early and delayed phases of H : M and washout rate also were significantly improved (P < 0.05) (from 2.59 to 2.63, from 2.12 to 2.27 and from 18.1 to 13.7%, respectively) in only group T.The change in SSPG was significantly correlated with the changes in H : M and washout rate (r = -0.639 and 0.577, respectively). Troglitazone had a beneficial effect on cardiac sympathetic nervous function through a decrease in insulin resistance in patients with essential hypertension.