The original aim of this study was to observe whether the depressor drug clonidine inhibited the abnormal hindquarter tone in spontaneously hypertensive rats (SHR). In conscious SHR and normotensive control rats (NCR), hindquarter (terminal aortic) blood flow was observed with an implantd electromagnetic flow probe and mean arterial pressure with an indwelling catheter. Twenty minutes after intravenous injection of clonidine (5 μg/kg) when arterial pressure reached a steady lower level, hindquarter resistance (HQR), calculated as mean arterial pressure divided by hindquarter flow, did not decrease in SHR. Thus we were unable to obtain evidence for an inhibitory effect of clonidine on the abnormal hindquarter tone in SHR. In NCR, HQR increased significantly by clonidine. The decrease in arterial pressure on clonidine was greater in SHR than in NCR, presumably because the increase in HQR partially offset the hypotensive effect in NCR. It seems that the increase in HQR in NCR was induced by a reflexive excitation of regional sympathetic vasoconstrictor fibers, which, being the final common path for the abnormal hindquarter tone also, were already being excited in SHR before clonidine administration. This point was quantitatively verified.