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Division of Cardiovascular Pathophysiology (A.F., P.M., J.D.) and Metabolic Research Laboratory (A.R., J.G.-A., G.F.), University of Navarra School of Medicine, and Departments of Endocrinology (J.S., G.F.) and Cardiology and Cardiovascular Surgery (J.D.), Clínica Universitaria de Navarra, 31008 Pamplona, Spain
Address all correspondence and requests for reprints to: Dr. G. Frühbeck, Department of Endocrinology, Clínica Universitaria de Navarra, 31008 Pamplona, Spain. E-mail: gfruhbeck{at}unav.es.
Besides its role in body weight control leptin may also act as a vasoactive hormone. This study was designed to investigate whether leptin modifies angiotensin II (ANG II)-induced vascular responses. The expression of functional leptin receptors (OB-Rb) was detected in vascular smooth muscle cells (VSMCs) from adult Wistar rats by RT-PCR. Immunocytochemistry and Western blot analysis further showed the expression of OB-R protein in VSMCs. The ANG II (10-7 mol/liter)-induced increase in intracellular Ca2+ was blocked (P < 0.01) by leptin (10-8 mol/liter). Moreover, in calcium-free buffer leptin was able to inhibit 65% of the ANG II-induced calcium release from intracellular stores. In endothelium-denuded aortic rings from adult Wistar rats no effect of leptin on basal tension was observed. However, the ANG II-induced isometric contraction was reduced (P < 0.05) by leptin (10-8 mol/liter). The experiments were also performed in age- and sex-matched Zucker rats, in which no effect of leptin on ANG II-induced calcium increase and vasoconstriction was observed. It is concluded that leptin blocks the vasoconstrictor action of ANG II and inhibits the ANG II-induced increase in intracellular Ca2+ in VSMCs through OB-Rb. These findings provide new insight into the physiological effects of leptin on blood pressure regulation.
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