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|Title:||Evidence for the existence of a constitutive nitric oxide synthase in vascular smooth muscle|
Nitric oxide synthase
Vascular smooth muscle
|Citation:||Cheah, L.S., Gwee, M.C.E., Das, R., Ballard, H., Yang, Y.F., Daniel, E.E., Kwan, C.Y. (2002). Evidence for the existence of a constitutive nitric oxide synthase in vascular smooth muscle. Clinical and Experimental Pharmacology and Physiology 29 (8) : 725-727. ScholarBank@NUS Repository. https://doi.org/10.1046/j.1440-1681.2002.03707.x|
|Abstract:||1. We have identified a neuronal nitric oxide synthase (NOS)-like constitutive form of NOS in vascular smooth muscle (VSM) using a functional contractility approach as well as immunohistochemical methods. 2. NG-Nitro-L-arginine methyl ester, NG-monomethyl-L-arginine and NG-nitro-L-arginine (L-NOARG), the competitive inhibitors of NOS, inhibited Mg2+-induced relaxation of de-endothelialized rat aorta precontracted with phenylephrine (PE). This Mg2+ relaxation of VSM was not affected by inhibitors of inducible NOS. 3. Electrical field stimulation (EFS; 30-70 Hz) caused relaxation of rat aorta in the presence of tetrodotoxin (therefore not a neurogenic effect) and this EFS relaxation was effectively inhibited by L-NOARG, oxyhemoglobin and methylene blue. 4. Immunohistochemical studies of dog saphenous vein using antibodies raised against neuronal NOS indicated prominent staining along the plasmalemma in a punctate pattern similar to the distribution of antibodies against caveolin-1, a major constituent of the plasmalemmal caveolae. 5. We propose that a constitutive NOS of non-endothelial, non-neuronal origin is present in a special caveolae domain of VSM cell membranes and could be activated by an ionic mechanism yet to be characterized.|
|Source Title:||Clinical and Experimental Pharmacology and Physiology|
|Appears in Collections:||Staff Publications|
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