1. The effect of different concentrations of phenoxybenzamine (0.1, 0.3, 1, 3, 10 and 30 nmoll -1) on the concentration-response curves to phenylephrine (a selective alpha 1-adrenoceptor agonist) and noradrenaline (a mixed alpha 1- and alpha 2-adrenoceptor agonist) was compared in two kinds of vascular tissue: dog saphenous vein (has both postsynaptic alpha 1- and alpha 2-adrenoceptors) and dog mesenteric and renal arteries--where only postsynaptic alpha 1-adrenoceptors have been shown to exist. 2. In the saphenous vein, where both alpha 1- and alpha 2-adrenoceptors coexist, at only one concentration of phenoxybenzamine, 3 nmoll -1, the concentration-response curve of noradrenaline was shifted to the right without a reduction of the maximum; and this shift was small (by 0.4 log units). 3. In tissues where only alpha 1-adrenoceptors exist postsynaptically (mesenteric and renal arteries) phenoxybenzamine never caused any shift of the noradrenaline concentration-response curves to the right without depressing the maximum effect. 4. In none of the tissues did phenoxybenzamine at any concentration shift the concentration-response curve of phenylephrine to the right without depressing its maximum. 5. All these results indicate that in the dog saphenous vein there is a 'false' alpha-adrenoceptor reserve for noradrenaline, since two kinds of receptors participate in the response to this amine. 6. The calculation of the occupancy-response relationship for the renal artery showed that 24% of the maximal response occurs when only 2% of alpha 1-adrenoceptors are activated and 50% of maximum at 9% occupation. However, for 95% of the maximal response an 83% occupancy is required. Similar values were calculated for the mesenteric artery. 7. Thus, the surplus alpha-adrenoceptors which is very large for a half-maximal response becomes smaller and smaller as the magnitude of the response increases and probably disappears at the 100% response level. 8. If we retain the original definition of 'spare receptors' - receptors in 'excess' of those required to produce a maximal response, we conclude, that there is no receptor reserve in the dog mesenteric and renal arteries.