The effect of systemic leptin administration on aorta smooth muscle responses in diabetic rats

• Published in: Molecular and cellular biochemistry 2006-01, Vol.282 (1-2), p.187-191
• Main Authors: Ozer, Ciğdem, Gülen, Sebnem, Dileköz, Ergin, Babül, Aydan, Ercan, Z Sevim
• Format: Article
• Language: English
• Subjects: Acetylcholine - pharmacology; Animals; Aorta, Thoracic - drug effects; Aorta, Thoracic - physiopathology; Central nervous system; Diabetes; Diabetes Mellitus, Experimental - physiopathology; Endothelium, Vascular - drug effects; Endothelium, Vascular - physiopathology; Endothelium-Dependent Relaxing Factors - metabolism; In Vitro Techniques; Leptin - administration & dosage; Leptin - pharmacology; Male; Muscle Contraction - drug effects; Muscle Contraction - physiology; Muscle, Smooth, Vascular - drug effects; Muscle, Smooth, Vascular - physiopathology; Nitric oxide; Nitric Oxide - metabolism; Phenylephrine - pharmacology; Rats; Rats, Wistar; Rodents; Vasoconstrictor Agents - pharmacology; Vasodilator Agents - pharmacology
• ISSN: 0300-8177; 1573-4919
• DOI: 10.1007/s11010-006-1927-0

Leptin produces effects in central nervous system and peripheral tissues via its specific receptors. Leptin also stimulates nitric oxide release in a concentration-dependent manner. In this study, our aim was to test the hypothesis that whether leptin has a modulatory role on endothelium or smooth muscle function in streptozotocin (STZ)-induced diabetic rats. Wistar-Albino rats were divided into four groups: 1 -- Control, 2 -- Diabetic, 3 -- Control + leptin and 4 -- Diabetic + leptin. Experimental diabetes was produced by intraperitoneal injection of a single dose of STZ (55 mg/kg). Diabetes was determined by increased fasting blood glucose level on the 7th day of the experiment. Leptin (0.1 mg/kg/day) was administered intraperitoneally for 5 days. At the end of the 5th day, thoracic aortas were isolated and phenylephrine (Phe)-induced contractions and acetylcholine (ACh)-induced relaxations of each group were estimated. In diabetic rats, Phe-induced contractility was increased (p < 0.05). Leptin pre-treatment increased the Phe-induced contractility significantly in aortic rings obtained from diabetic rats (p < 0.05). In normal rats, leptin administration produced only a slight and non-significant increase in Phe-induced contractions. Although the relaxant responses were decreased in diabetic rats, leptin administration enhanced the ACh-induced relaxation in both normal and diabetic animals significantly. As a conclusion; chronic leptin pre-treatment caused a significant increase both in Phe-induced contractions and ACh-induced Endothelial-Derived Relaxing Factor (EDRF)/Nitric oxide-mediated relaxations in the aortic rings isolated from streptozotocin-induced diabetic rats. This peptide hormone caused a significant increase in the relaxations obtained by ACh while not inducing a significant alteration in the contractile effect of Phe in control rats.