General Physiology and Biophysics Vol.31, No.4, p.409–413, 2012
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Title: Mg2+-induced adenosine-receptor mediated relaxations in mesenteric vascular beds of diabetic rats |
Author: Roya Amiri Tavasoli, Nepton Soltani, Mansoor Keshavarz, Shahla Shorabipour |
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Abstract: Our previous studies showed that the magnesium Mg2+-induced relaxations were completely dependent on concentration of nitric oxide (NO) in non-diabetic rat mesenteric vascular beds, in diabetic rats other mechanisms may be involved. The present study was designed to determine the role of adenosine receptor in Mg2+-induced relaxation in streptozotocin (STZ)-induced diabetic rats vessels. Diabetes was induced by the intravenous injection of 60 mg/kg STZ. Eight weeks after diabetes induction, superior mesenteric arteries were isolated and perfused according to the McGregor method. Prepared vascular beds were constricted with phenylephrine to induce 70–75% of maximal constriction (0.001 M). Mg2+ at concentrations of 10–4 to 10–1 M were added into the medium and perfusion pressure was recorded. Theophylline (1 mM), and 3,7- dimethyl-1- propargylxanthine (0.01 μM) were added into medium 20 min before phenylephrine administration. In the presence of theophylline, vasorelaxation induced by high dose of Mg2+ (from 0.03 to 0.1 M) was totally suppressed. In presence of N(ω)-nitro-L-arginine methyl ester (L-NAME), the response of Mg2+ was completely inhibited at low dose of Mg2+. But, Mg2+-induced relaxation in the presence of adenosine A2a receptor blocker was significantly suppressed in high dose of Mg2+. Mg2+-induced relaxation in the presence of an A2a receptor blocker was not suppressed either by denudation of endothelium or presence of L-NAME. From the results of this study it may be concluded that Mg2+-induced relaxation at high concentrations is mediated by adenosine A2a receptors, but at low concentrations Mg2+-induced relaxation is dependent on NO.
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Keywords: Diabetes — Magnesium — Adenosine A2a receptor — Nitric oxide — Mesenteric bed |
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Year: 2012, Volume: 31, Issue: 4 |
Page From: 409, Page To: 413 |
doi:10.4149/gpb_2012_050
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