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the reduced amount of kinin suppresses extravasation ' . In contrast, raising the kinin level in the ascites by administering enarapril, an ACE inhibitor, increased the volume of the ascitic fluid accumulation (Figure 5) 11-14.

Figure 4. Kinin generating cascade and various vascular mediators in cancer tissues affecting the EPR effect. Mediators, enzymes, and inhibitors are shown. See text for details. M<(>, macrophage; PMN, polymorphonuclear cells; COXs, cyclooxygenases; PGs, prostaglandins. SBTI, soybean trypsin inhibitor (Kunitz type); ONOCT, peroxynitrite; NO, nitric oxide;

Figure 4. Kinin generating cascade and various vascular mediators in cancer tissues affecting the EPR effect. Mediators, enzymes, and inhibitors are shown. See text for details. M<(>, macrophage; PMN, polymorphonuclear cells; COXs, cyclooxygenases; PGs, prostaglandins. SBTI, soybean trypsin inhibitor (Kunitz type); ONOCT, peroxynitrite; NO, nitric oxide;

Figure 5. Enhanced extravasation and accumulation of 51Cr-labeled albumin in the peritoneal cavity of mice with ascitic S-180 tumor. Each agent was administrated orally. Data are expressed as means ±S.E., n = 5. See text for details. Adapted from Ref. 12. * P < 0.05; ** P < 0.01 (versus control).

Figure 5. Enhanced extravasation and accumulation of 51Cr-labeled albumin in the peritoneal cavity of mice with ascitic S-180 tumor. Each agent was administrated orally. Data are expressed as means ±S.E., n = 5. See text for details. Adapted from Ref. 12. * P < 0.05; ** P < 0.01 (versus control).

We recently showed that another ACE inhibitor, temocapril, selectively suppressed blood flow in tumor, whereas blood flow in the kidney, the liver,

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