α-Adrenoceptor coupling to polyphosphoinositide (PI) hydrolysis was studied in the rat tail artery. Inositol phosphate (IP) accumulation was stimulated by the non-selective α-adrenoceptor agonist norepinephrine and the α1-adrenoceptor agonist phenylephrine. This stimulation was relatively dependent on extracellular Ca2+ and enhanced markedly in the presence of LiCl. In addition, norepinephrine- and phenylephrine-stimulated IP accumulation was relatively sensitive to blockade by prazosin, compared to rauwolscine. The putative α2-adrenoceptor agonist UK 14304 also stimulated PI breakdown in a concentration-dependent manner, although this stimulation did not reach equilibrium at up to 10 mM and was relatively sensitive to prazosin, compared to rauwolscine, over the lower agonist concentrations. NaF stimulated IP accumulation independently of α-adrenoceptor activation. PI breakdown by α-adrenoceptor agonists and NaF was attenuated by N-ethylmaleimide but not pertussis toxin treatment. In addition, dithiothreitol blocked NaF-stimulated, but not α-adrenoceptor-mediated, PI breakdown. These results suggest the coupling of α1-adrenoceptor, via phospholipase C, to PI hydrolysis in the rat tail artery. This study also provides evidence for the involvement of one or more non-Gi-like G-protein(s) in the signal transduction process.
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