A KALLIKREIN-LIKE ENZYME IN BLOOD-VESSELS OF ONE-KIDNEY, ONE CLIP HYPERTENSIVE RATS

Active and inactive kallikrein or a kallikrein-like enzyme are found in the aorta, vena cava, and tail artery and veins of the rat. We studied the concentration of vascular kininogenase in rats with one-kidney, one clip renovascular hypertension and in unilaterally nephrectomized normotensive rats. Six weeks after surgery, active and total vascular kininogenase activity (active plus trypsin-activated) was measured. Blood pressure was 212 ± 4 mm Hg in the hypertensive rats (n = 33) and 120 ± 1 mm Hg in the normotensive rats (n = 32) (p < 0.001). Active kininogenase was lower in the hypertensive rats; although the difference was not significant in the thoracic aorta (56 ± 8 versus 77 ± 15), it was highly signficant in the abdominal aorta (63 ± 13 versus 167 ± 17, p < 0.001) and tail artery (48 ± 8 versus 197 ± 31, p < 0.003). Total vascular kininogenase activity (active plus trypsin-activated) was lower in the hypertensive rats in all arteries examined: thoracic aorta (183 ± 16 versus 380 ± 38, p < 0.003), abdominal aorta (565 ± 61 versus 1,093 ±74, p < 0.001), and tail artery (532 ± 112 versus 1,243 ± 135, p < 0.003). Active kininogenase in the vena cava was higher in the hypertensive rats (213 ± 56 versus 131 ± 31); however, this difference was not statistically significant, whereas in the tail veins it was highly significant (1,803 ± 221 versus 771 ± 79, p < 0.003). Total venous kininogenase activity was significantly higher in the hypertensive rats (vena cava, 1.850 ± 171 versus 998 ± 149, p < 0.01; tail vein, 4,261 ± 261 versus 2,521 ± 212, p < 0.001). In conclusion, we found that in rats with one-kidney, one clip renovascular hypertension both active and total vascular kininogenase are decreased in the arteries and increased in veins. These changes may contribute to the pathogenesis of hypertension.