Tumor-selective blood flow decrease induced by an angiotensin converting enzyme inhibitor, temocapril hydrochloride

Japanese Journal of Cancer Research

Volumn 91, Issue 2, 2000, Pages 261-269

  Hori, Katsuyoshi ^a   Saito, Sachiko ^a   Takahashi, Hiroto ^b   Sato, Haruhiko ^c   Maeda, Hiroshi ^d   Sato, Yasufumi ^a  

^a TOHOKU UNIVERSITY   (Japan)

^b Department of Internal Medicine   (Japan)

^c Sendai Shakaihoken Hospital   (Japan)

^d KUMAMOTO UNIV SCHOOL OF MEDICINE   (Japan)

Author keywords

ACE inhibitor; Angiotensin II; Drug delivey system; Temocapril hydrochloride; Tumor blood flow

Indexed keywords

ANGIOTENSIN; DIPEPTIDYL CARBOXYPEPTIDASE INHIBITOR; TEMOCAPRIL;

ANIMAL EXPERIMENT; ANTINEOPLASTIC ACTIVITY; ARTICLE; BONE MARROW; BRAIN BLOOD FLOW; CONTROLLED STUDY; DRUG SELECTIVITY; DRUG TRANSPORT; HUMAN; HUMAN CELL; KIDNEY BLOOD FLOW; LIVER BLOOD FLOW; NONHUMAN; PRIORITY JOURNAL; TUMOR BLOOD FLOW; TUMOR VOLUME; YOSHIDA SARCOMA;

EID: 0034009815     PISSN: 09105050     EISSN: None     Source Type: Journal    
DOI: 10.1111/j.1349-7006.2000.tb00940.x     Document Type: Article

References (40)

1. Suzuki, M., Hori, K., Abe, I., Saito, S. and Sato, H. Functional characterization of the microcirculation in tumors. Cancer Metastasis Rev., 3, 115-126 (1984).
2. Chaplin, D. J., Horsman, M. R., Trotter, M. J. and Siemann, D. W. Therapeutic significance of microenvironmental factors. In "Blood Perfusion and Microenvironment of Human Tumors: Implications for Clinical Radiooncology," ed. P. Vaupel and M. Molls, pp. 133-143 (1998). Springer, Berlin.
3. Song, C. W. Modification of blood flow. In "Blood Perfusion and Microenvironment of Human Tumors: Implications for Clinical Radiooncology," ed. P. Vaupel and M. Molls, pp. 193-207 (1998). Springer, Berlin.
4. Suzuki, M. Selective increase in intratumoral concentration of anticancer drugs and extension of retention time based on two functional characteristics of tumor vessels. Adv. Cancer Treat., 7, 77-81 (1988) (in Japanese).
5. Pruijn, F. B., van Daalen, M., Holford, N. H. G. and Wilson, W. R. Mechanisms of enhancement of the antitumour activity of melphalan by the tumour-blood-flow inhibitor 5,6-dimethylxanthenone-4-acetic acid. Cancer Chemother. Pharmacol., 39, 541-546 (1997).
6. Suzuki, M., Hori, K., Abe, I., Saito, S. and Sato, H. A new approach to cancer chemotherapy. Selective enhancement of tumor blood flow with angiotensin II. J. Natl. Cancer Inst., 67, 663-669 (1981).
7. Abe, I., Hori, K., Saito, S., Tanda, S., Li, Y. and Suzuki, M. Increased intratumor concentration of fluorescein-isothiocyanate-labeled neocarzinostatin in rats under angiotensin-induced hypertension. Jpn. J. Cancer Res. (Gann), 79, 874-879 (1988).
8. Sato, H., Sugiyama, K., Hoshi, M., Urushiyama, M. and Ishizuka, K. Angiotensin II (AII) induced hypertension chemotherapy (IHC) for unresectable gastric cancer: with reference to resection after down staging. World J. Surg., 19, 836-842 (1995).
9. Algire, G. H., Legallais, F. Y. and Anderson, B. F. Vascular reaction of normal and malignant tissue in vivo. VI. The role of hypotension in the action of components of podophyllin on transplantable sarcomas. J. Natl. Cancer Inst., 14, 879-893 (1954).
10. Cater, D. B., Grigson, C. M. B. and Watkinson, D. A. Changes of oxygen tension in tumours induced by vasoconstrictor and vasodilator drugs. Acta Radiol., 58, 401-434 (1962).
11. Peters, C. E. and Chaplin, D. J. Blood flow modification in the SCCVII tumor: effects of 5-hydroxytryptamine, hydralazine, and propranolol. Int. J. Radiat. Oncol. Biol. Phys., 22, 463-465 (1992).
12. Chaplin, D. J. and Acker, B. The effect of hydralazine on the tumor cytotoxicity of the hypoxic cell cytotoxin RSU-1069: evidence for therapeutic gain. Int. J. Radiat. Oncol. Biol. Phys., 13, 579-585 (1987).
13. 4AN tumors and normal tissues in rats. Int. J. Radiat. Oncol. Biol. Phys., 36, 393-401 (1996).
14. Hill, S., Williams, K. B. and Denekamp, J. Vascular collapse after flavone acetic acid: a possible mechanism of its anti-tumor action. Eur. J. Cancer Clin. Oncol., 25, 1419-1424 (1989).
15. Bibby, M. C., Double, J. A., Loadman, P. M. and Duke, C. V. Reduction of tumor blood flow by flavone acetic acid: a possible component of therapy. J. Natl. Cancer Inst., 81, 216-220 (1989).
16. Zwi, L. J., Baguley, B. C., Gavin, J. B. and Wilson, W. R. Blood flow failure as a major determinant in the antitumor action of flavone acetic acid. J. Natl. Cancer Inst., 81, 1005-1013 (1989).
17. Kallinowski, F., Shaefer, C., Tyler, G. and Vaupel, P. In vivo targets of recombinant human tumour necrosis factor - blood flow, oxygen consumption and growth of isotransplanted rat tumours. Br. J. Cancer. 60, 555-560 (1989).
18. Baguley, B. C., Holdaway, K. M., Thomsen, L. L., Zhuang, L. and Zwi, L. J. Inhibition of growth of colon 38 adenocarcinoma by vinblastine and colchicine: evidence for a vascular mechanism. Eur. J. Cancer, 27, 482-487 (1991).
19. Hill, S. A., Lonergan, S. J., Denekamp, J. and Chaplin, D. J. Vinca alkaloids: anti-vascular effects in a murine tumor. Eur. J. Cancer, 29A, 1320-1324 (1993).
20. Cliffe, S., Taylor, M. L., Rutland, M., Baguley, B. C., Hill, R. P. and Wilson, W. R. Combining bioreductive drugs (SR 4233 or SN 23862) with the vasoactive agents flavone acetic acid or 5,6-dimethylxanthenone acetic acid. Int. J. Radiat. Oncol. Biol. Phys., 29, 373-377 (1994).
21. Tozer, G. M., Prise, V. E. and Chaplin, D. J. Inhibition of nitric oxide synthase induces a selective reduction in tumor blood flow that is reversible with L-arginine. Cancer Res., 57, 948-955 (1997).
22. Dark, G. D., Hill, S. A., Prise, V. E., Tozer, G. M., Pettit, G. R. and Chaplin, D. J. Combretastatin A-4, an agent that displays potent and selective toxicity toward tumor vasculature. Cancer Res., 57, 1829-1834 (1997).
23. Tozer, G. M., Prise, V. E., Wilson, J., Locke, R. J., Vojnovic, B., Stratford, M. R. L., Dennis, M. F. and Chaplin, D. J. Combretastatin A-4 phosphate as a tumor vascular-targeting agent: early effects in tumors and normal tissues. Cancer Res., 59, 1626-1634 (1999).
24. Hori, K., Saito, S., Nihei, Y., Suzuki, M. and Sato, Y. Antitumor effects due to irreversible stoppage of tumor tissue blood flow: evaluation of a novel combretastatin A-4 derivative, AC7700. Jpn. J. Cancer Res., 90, 1026-1038 (1999).
25. Hori, K., Suzuki, M., Tanda, S. and Saito, S. In vivo analysis of tumor vascularization in the rat. Jpn. J. Cancer Res., 81, 279-288 (1990).
26. Hori, K., Suzuki, M., Tanda, S., Saito, S., Shinozaki, M. and Zhang, Q.-H. Fluctuations in tumor blood flow under normotension and the effect of angiotensin II-induced hypertension. Jpn. J. Cancer Res., 82, 1309-1316 (1991).
27. Hori, K., Zhang, Q.-H., Li, H.-C., Saito, S. and Sato, Y. Timing of cancer chemotherapy based on circadian variations in tumor tissue blood flow. Int. J. Cancer, 65, 360-364 (1996).
28. Aukland, K., Bower, B. F. and Berliner, R. W. Measurement of local blood flow with hydrogen gas. Circ. Res., 14, 164-187 (1964).
29. Hori, K., Zhang, Q.-H., Saito, S., Tanda, S., Li, H.-C. and Suzuki, M. Microvascular mechanisms of change in tumor blood flow due to angiotensin II, epinephrine, and methoxamine: a functional morphometric study. Cancer Res., 53, 5528-5534 (1993).
30. Sitzmann, J. V., Wu, Y. and Cameron, J. L. Altered angiotensin-II receptors in human hepatocellular and hepatic metastatic colon cancers. Ann. Surg., 219, 500-507 (1994).
31. Marsigliante, S., Resta, L., Muscella, A., Vinson, G. P., Marzullo, A. and Storelli, C. AT1 angiotensin II receptor subtype in the human larynx and squamous laryngeal carcinoma. Cancer Lett., 110, 19-27 (1996).
32. Wu, Y., Cahill, P. A. and Sitzmann, J. V. Decreased angiotensin II receptors mediate decreased vascular response in hepatocellular cancer. Ann. Surg., 223, 225-231 (1996).
33. Opocher, G., Rocco, S., Cimolato, M., Vianello, B., Arnaldi, G. and Mantero, F. Angiotensin II receptors in cortical and medullary adrenal tumors. J. Clin. Endocrinol. Metab., 82, 865-869 (1997).
34. Kohzuki, M., Tanda, S., Hori, K., Yoshida, K., Kamimoto, M., Wu, X. M. and Sato, T. Endothelin receptors and angiotensin II receptors in tumor tissue. J. Cardiovasc. Pharmacol., 31 (Suppl. 1), S531-533 (1998).
35. Matsumura, Y. and Maeda, H. A new concept for macromolecular therapeutics in cancer chemotherapy: mechanism of tumoritropic accumulation of proteins and the antitumor agent Smancs. Cancer Res., 46, 6387-6392 (1986).
36. Maeda, H. SMANCS and polymer-conjugated macromolecular drugs: advantages in cancer chemotherapy. Adv. Drug Delivery Rev., 6, 181-202 (1991).
37. Maeda, H. and Miyamoto, Y. SMANCS approach - oily formulations of protein drugs for arterial injection and oral administration. In "Drug Absorption Enhancement Concepts, Possibilities, Limitations and Trends," ed. A. G. de Boer, pp. 221-247 (1994). Harwood Academic Publ., Switzerland.
38. Stratford, I. J., Adams, G. E., Godden, J., Nolan, J., Howells, N. and Timpson, N. Potentiation of the antitumour effect of melphalan by the vasoactive agent, hydralazine. Br. J. Cancer, 58, 122-127 (1988).
39. Quinn, P. K., Bibby, M. C., Cox, J. A. and Crawford, S. M. The influence of hydralazine on the vasculature, blood perfusion and chemosensitivity of MAC tumours. Br. J. Cancer, 66, 323-330 (1992).
40. Parkins, C. S., Denekamp, J. and Chaplin, D. J. Enhancement of mitomycin-C cytotoxicity by combination with flavone acetic acid in a murine tumour. Anticancer Res., 13, 1437-1442 (1993).