Noradrenaline stimulation of high-affinity GTPase activity in membranes from rat aorta and caudal artery

The ability of noradrenaline (NA) to stimulate increases in high-affinity GTPase activity in sarcolemma-enriched rat aorta and caudal artery membranes was examined in the present study. In aortic membranes, NA significantly (P < 0.05; N = 5) increased the V-max from a basal value of 103 +/- 29 to 156 +/- 38 pmol P-i/min/mg protein, but did not affect the K-m which was 0.32 +/- 0.08 mu M in the absence and 0.58 +/- 0.16 mu M in the presence of NA. However, in caudal artery membranes, NA significantly (P < 0.05; N = 6) increased both the V-max and the K-m from basal values of 69 +/- 12 pmol P-i/min/mg protein and 0.24 +/- 0.05 mu M, respectively, to 205 +/- 54 pmol P-i/min/mg protein and 1.01 +/- 0.25 mu M, respectively. Removing the endothelium from both artery preparations did not alter significantly basal GTPase activity or the magnitude of the increase stimulated by NA. Prazosin significantly inhibited NA-stirnulated increases in GTPase activity in membranes from endothelium-denuded caudal artery and aorta, and in endothelium-intact caudal artery membranes. However, yohimbine significantly inhibited NA-stimulated increases in GTPase activity only in preparations from endothelium-intact caudal arteries. Therefore, in endothelium-intact caudal artery membranes, NA stimulated increases in GTPase activity that were apparently mediated by both alpha(1)-adrenoceptors and alpha(2)-adrenoceptors, while in endothelium-denuded aortic and caudal artery membranes this increase was mediated solely by oc,adrenoceptors. Western blotting of these arteries confirmed the presence of both G(i alpha 2,3) and G(q/11 alpha), which are candidates for mediating the alpha(1)-adrenocepeor-stimulated increases in GTPase activity.