WHY IS THE HYPOTENSIVE EFFECT OF CLONIDINE GREATER IN HYPERTENSIVE RATS

The original aim of this study was to observe whether the depressor dr ug clonidine inhibited the abnormal hindquarter tone in spontaneously hypertensive rats (SHR). In conscious SHR and normotensive control rat s (NCR), hindquarter (terminal aortic) blood flow was observed with an implantd electromagnetic flow probe and mean arterial pressure with a n indwelling catheter. Twenty minutes after intravenous injection of c lonidine (5 mu g/kg) when arterial pressure reached a steady lower lev el, hindquarter resistance (HQR), calculated as mean arterial pressure divided by hindquarter flow, did not decrease in SHR. Thus we were un able to obtain evidence for an inhibitory effect of clonidine on the a bnormal hindquarter tone in SHR. In NCR, HQR increased significantly b y clonidine. The decrease in arterial pressure on clonidine was greate r in SHR than in NCR, presumably because the increase in HQR partially offset the hypotensive effect in NCR. It seems that the increase in H QR in NCR was induced by a reflexive excitation of regional sympatheti c vasoconstrictor fibers, which, being the final common path for the a bnormal hindquarter tone also, were already being excited in SHR befor e clonidine administration. This point was quantitatively verified. (C ) 1997 Tohoku University Medical Press.