SUMMARY Although the existence of so-called streptozocin hypertension seems well established, some reports have indicated that no rise in blood pressure (BP) occurred after streptozocin treatments. To ascertain the streptozocin-induced BP response, normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) were treated with streptozocin, 40 to 45 and 35 mg/kg i. v., respectively, and BP was determined directly and indirectly every week for 3 to 4 weeks. Direct mean BP was determined without anesthesia or restraint through a cannula inserted into the rat's abdominal aorta. Indirect BP was determined at the tail without anesthesia after prewarming the rat in a holder. Compared with control values, indirect BP increased significantly in diabetic WKY 2 weeks after streptozocin treatment. In contrast, direct BP of these rats decreased, compared with control values. Indirect BP of diabetic SHR was as high as that of the controls, whereas direct BP of diabetic SHR decreased significantly 1 week after the treatment and thereafter, compared with control values. These discrepancies between the direct and indirect BP values may be caused by severe emaciation of diabetic rats. Extra pressure in the cuff may be necessary to occlude the bloodstream. These results indicate that under these conditions the value of BP obtained by the direct measurement is more reliable than that by the indirect one; therefore, we concluded that so-called streptozocin hypertension does not exist. (Hypertension 10: 517-521, 1987 Received May 20, 1987; accepted June 25, 1987. been suggested to play a role in the development of hypertension in STZ-induced diabetic rats. On the other hand, some reports do not support the existence of hypertension in STZ-diabetic rats. 78 Somani et al. 9 reported that blood pressure (BP) in Wistar-Kyoto rats (WKY) rises progressively with increasing dose of STZ, whereas STZ induces a dose-dependent decrease of BP in spontaneously hypertensive rats (SHR). Rodgers et al. 10 reported that STZ induces a depressor effect in SHR and has no effect in WKY. Of these groups, 1 " 10 only two tried to determine BP directly. 3 -9 All other groups determined BP using the indirect tailcuff measurement. In a previous study, in which we tried to develop an animal model of hypertension with diabetes mellitus, we found a discrepancy between BP values determined by direct cannulation and the indirect tail-cuff method.11 In Wistar rats, WKY, and SHR treated with STZ (30-80 mg/kg i.v.), the indirect BP measurement yielded hypertensive values whereas rather low BP values were obtained by the direct measurement.11 To our knowledge, no previous study has conducted parallel determinations of direct and indirect BP in STZ-