Publicaciones científicas

Leptin inhibits angiotensin II-induced intracellular calcium increase and vasoconstriction in the rat aorta

01-sep-2002 | Revista: Endocrinology

Fortuño A., Rodríguez A., Gómez-Ambrosi J., Muñiz P., Salvador J., Díez J., Frühbeck G.
Division of Cardiovascular Pathophysiology, University of Navarra School of Medicine, Pamplona, Spain

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 Ca(2+) 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 Ca(2+) in VSMCs through OB-Rb.

These findings provide new insight into the physiological effects of leptin on blood pressure regulation.

CITA DEL ARTÍCULO Endocrinology. 2002 Sep;143(9):3555-60