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 Vmax from a basal value of 103 +/- 29 to 156 +/- 38 pmol Pi/min/mg protein, but did not affect the Km which was 0.32 +/- 0.08 microM in the absence and 0.58 +/- 0.16 microM in the presence of NA. However, in caudal artery membranes, NA significantly (P < 0.05; N = 6) increased both the Vmax and the Km from basal values of 69 +/- 12 pmol Pi/min/mg protein and 0.24 +/- 0.05 microM, respectively, to 205 +/- 54 pmol Pi/min/mg protein and 1.01 +/- 0.25 microM, 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-stimulated 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 alpha 1-adrenoceptors. Western blotting of these arteries confirmed the presence of both Gi alpha 2,3 and Gq/11 alpha, which are candidates for mediating the alpha 1-adrenoceptor-stimulated increases in GTPase activity.