Volume 13, Issue 2 (Summer 2009)                   Physiol Pharmacol 2009, 13(2): 151-159 | Back to browse issues page

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Golmohammadi M, Hajizadeh S, Faghihi M, Hosein M, Rohampour K. The Role of NO and cGMP in vasodilatory effect of β2-adrenoceptors in rat skin. Physiol Pharmacol 2009; 13 (2) :151-159
URL: http://ppj.phypha.ir/article-1-489-en.html
Abstract:   (11232 Views)
Introduction: In recent study both endothelium-dependent and endothelium-independent mechanisms have been reported for the action of β-adrenoceptor. The aim of this study was to investigate on the role of nitric oxide (NO) and cyclic guanosin monophosphate (cGMP) in vasodilation mechanisms of β2-adrenoceptors (β2-AR) in rat skin vessels. Methods: All drugs were injected subcutaneous into planar skin of hind paw. Injection volume was 10µl (5µl/min). Induction of anesthesia was perform with urethane 1.5 g/kg. Laser Doppler Flowmetery (LDF) technique was used for skin blood flow (SBF) monitoring. Results: The results obtained in this study showed that different doses of salbutamol, selective β2-AR agonist (1µM) caused a significant increase of SBF, but there was not any significant different in the response of different doses. Atenolol, selective β1-adrenoceptor antagonist (10µM) alone and with salbutamol had no significant effect on SBF. Propranolol, non selective β-adrenoceptor antagonist (1µM) by itself did not changed SBF, but significantly reduced the vasodilatory effect of salbutamol. LNNA, NO inhibitor (10µM) and methylen blue, cGMP inhibitor (3µM) caused a significant decrease of SBF 6/95% and 7/91% respectively. Salbutamol injection after LNNA and NO raised the SBF to 24/7% and 22.5% respectively, which shows a significant reduction in comparison to salbutamol’s effect (42.73%). Conclusion: The results indicated that, salbutamol dilate rat skin vessels via β2- ARs. NO and cGMP involved in β2-ARs mediated vasodilation and contribute to regulation of vascular skin tone. To elucidate the exact mechanism of this response more studies are needed.
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