The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

Beta-adrenoceptor-mediated relaxation inhibited by tetrapentylammonium ions in rat mesenteric artery.

The aim of this study was to examine the contribution of K+ channel activation to beta-adrenoceptor-mediated relaxation in rat mesenteric arteries. Isoprenaline and fenoterol concentration-dependently relaxed the phenylephrine-preconstricted endothelium-intact arteries of the rat with EC50 values of 0.26 +/- 0.03 microM and 0.87 +/- 0.12 microM, respectively. Beta-adrenoceptor-mediated relaxation was significantly attenuated upon removal of endothelium. Tetrapentylammonium ions (TPA+) at low concentrations (1-5 microM) inhibited relaxations induced by beta-adrenoceptor agonists in arteries with and without endothelium, while glibenclamide (3 microM) had no effect. TPA+ (5 microM) inhibited isoprenaline-induced relaxation in the presence of either iberiotoxin (100 nM) or glibenclamide (3 microM). TPA+ did not alter forskolin-induced relaxation. In the presence of 60 mM extracellular K+, the relaxations induced by two agonists were reduced in endothelium-intact arteries and abolished in endothelium-denuded arteries. The present results suggest that the activation of TPA+-sensitive K+ channels contributes toward the relaxations mediated through beta- and beta2-adrenoceptor stimulation in rat mesenteric arteries.[1]

References

 
WikiGenes - Universities