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1 Muscle Metabolism Laboratory, Department of Physiology, University of Arizona College of Medicine, Tucson, Arizona 85721-0093; and 2 Hypertension and Diabetes Research Unit, Max-Grundig-Klinik, 77815 Bühl, Germany
Acute
administration of the angiotensin-converting enzyme (ACE) inhibitor
captopril enhances insulin-stimulated glucose transport activity in
skeletal muscle of the insulin-resistant obese Zucker rat. The present
study was designed to assess whether this effect is mediated by an
increase in the nonapeptide bradykinin (BK), by a decrease in action of
ANG II, or both. Obese Zucker rats (8-9 wk old) were
treated for 2 h with either captopril (50 mg/kg orally), bradykinin
(200 µg/kg ip), or the ANG II receptor
(AT1 subtype) antagonist
eprosartan (20 mg/kg orally). Captopril treatment enhanced in vitro
insulin-stimulated (2 mU/ml) 2-deoxyglucose uptake in the
epitrochlearis muscle by 22% (251 ± 7 vs. 205 ± 9 pmol · mg
1 · 20 min1;
P < 0.05), whereas BK treatment
enhanced this variable by 18% (249 ± 15 vs. 215 ± 7 pmol · mg1 · 20 min1;
P < 0.05). Eprosartan did
not significantly modify insulin action. The BK-mediated increase in
insulin action was completely abolished by pretreatment with either the
specific BK-B2 receptor antagonist HOE 140 (200 µg/kg ip) or the nitric oxide synthase inhibitor N
-nitro-L-arginine methyl ester
(50 mg/kg ip). Collectively, these results indicate that the modulation
of insulin action by BK likely underlies the metabolic effects of ACE
inhibitors in the insulin-resistant obese Zucker rat. Moreover, this
modulation of insulin action by BK is likely mediated through
B2 receptors and by an increase in
nitric oxide production and/or action in skeletal muscle tissue.
obese Zucker rat; epitrochlearis muscle; 2-deoxyglucose uptake
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