In recent studies, both endothelium-dependent and endothelium-independent mechanisms have been reported for the action of β-adrenoceptors. The aim of this study was to investigate the role of nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) in β 2 -adrenoceptors (β 2 -AR) mediated vasodilation in rat skin vessels. Methods: All drugs were injected subcutaneously into the plantar skin of the hind paw. Injection volume was 10 µl (5µl/min). Induction of anesthesia was performed with

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... ane 1.5 g/kg. Laser Doppler Flowmetery (LDF) technique was used to monitor the skin blood flow (SBF). Results: The results obtained in this study showed that different doses of salbutamol, a selective β 2 -AR agonist (1µM), caused a significant increase of SBF, but effects induced by different doses of salbutamol were not significantly different. Atenolol, a selective β1-adrenoceptor antagonist (10 µM), alone and with salbutamol had no significant effect on SBF. Propranolol, a non selective β-adrenoceptor antagonist (1 µM), did not changed SBF by itself, but significantly reduced the vasodilatory effect of salbutamol. LNNA, a NO inhibitor (10µM) and methylen blue, a cGMP inhibitor (3µM), caused significant decreases in SBF equal to 6.95% and 7.91%, respectively. Salbutamol injection after LNNA and NO raised the SBF to 24.7% and 22.5%, respectively. These values were significantly lower than the value observed for salbutamol (42.73%). Conclusion: The results indicated that, salbutamol dilates rat skin vessels via β 2 -ARs. NO and cGMP are involved in β 2 -ARs mediated vasodilation and contributed to the regulation of skin vascular tone. More studies are required to elucidate the exact mechanism of function of β 2 -adrenoceptors.