

An Indispensible Parameters of Trandolapril Include Indications, Pharmaco Dynamics, Actions, Route of Excretion, Half-Life Toxicity and Interactions
Abstract
Trandolapril is a non-sulfhydryl prodrug that is associated with the angiotensin-converting enzyme (ACE) inhibitor of medications. It is metabolized to its biologically active diacid form, trandolaprilat, especially in the liver. The enzyme ACE, which is necessary for the transformation of angiotensin I (ATI) into angiotensin II (ATII), is inhibited by trendolaprilat. A vital part of the renin-angiotensin-aldosterone system (RAAS), ATII regulates blood pressure. Trandolapril plays an important role regarding treatment of mild to moderate hypertension, to promote survival following myocardial infarction in stable patients in a clinical manner along with left ventricular dysfunction, as an adjunct treatment for congestive heart failure, and to reduce the rate of progression of renal disease in hypertensive individuals along with diabetes mellitus and microalbuminuria or overt nephropathy.
References
Joshi, N., Bhirud, S., Ramam, B., & Bodkhe, A. (2006). Process for the preparation of intermediates of trandolapril and use thereof for the preparation of trandolapril (U.S. Patent No. US 20060079698). U.S. Patent and Trademark Office.
Coresh, J., Selvin, E., Stevens, L. A., Manzi, J., Kusek, J. W., Eggers, P., Van Lente, F., & Levey, A. S. (2007). Prevalence of chronic kidney disease in the United States. JAMA, 298(17), 2038–2047. https://doi.org/10.1001/jama.298.17.2038
White, S. L., Cass, A., Atkins, R. C., Chadban, S., & Brown, W. (2005). Chronic kidney disease in the general population. Advances in Chronic Kidney Disease, 12(1), 5–13. https://doi.org/10.1053/j.ackd.2004.10.009
Schieppati, A., & Remuzzi, G. (2005). Chronic renal diseases as a public health problem: Epidemiology, social, and economic implications. Kidney International Supplement, 98, S7–S10. https://doi.org/10.1111/j.1523-1755.2005.09801.x
Eknoyan, G., Lameire, N., Barsoum, R., Eckardt, K., Levin, A., Levin, N., & Johnson, C. (2004). The burden of kidney disease: Improving global outcomes. Kidney International, 66(4), 1310–1314. https://doi.org/10.1111/j.1523-1755.2004.00894.x
Brenner, B. M., Cooper, M. E., de Zeeuw, D., Keane, W. F., Mitch, W. E., Parving, H. H., Remuzzi, G., Snapinn, S., Zhang, Z., & Shahinfar, S. (2001). Effects of losartan on renal and cardiovascular outcomes in patients with type 2 diabetes and nephropathy. The New England Journal of Medicine, 345(12), 861–869. https://doi.org/10.1056/NEJMoa011161
Hou, F. F., Zhang, X., Zhang, G. H., Xie, D., Chen, P., Zhang, W. J., Li, X. Q., Zhou, X., Wang, G. B., & Huang, F. (2006). Efficacy and safety of benazepril for advanced chronic renal insufficiency. The New England Journal of Medicine, 354(2), 131–140. https://doi.org/10.1056/NEJMoa053107
Müller, D. N., & Luft, F. C. (2006). Direct renin inhibition with aliskiren in hypertension and target organ damage. Clinical Journal of the American Society of Nephrology, 1(2), 221–228. https://doi.org/10.2215/CJN.01201005
Nguyen, G., & Contrepas, A. (2008). Physiology and pharmacology of the (pro)renin receptor. Current Opinion in Pharmacology, 8(2), 127–132. https://doi.org/10.1016/j.coph.2007.12.009
Nguyen, G., Delarue, F., Burcklé, C., Bouzhir, L., Giller, T., & Sraer, J. (2002). Pivotal role of the renin/prorenin receptor in angiotensin II production and cellular responses to
renin. Journal of Clinical Investigation, 109(11), 1417–1427. https://doi.org/10.1172/JCI14276
Liu, Y. (2006). Renal fibrosis: New insights into the pathogenesis and therapeutics. Kidney International, 69(2), 213–217. https://doi.org/10.1038/sj.ki.5000054
Eddy, A. A. (2005). Progression in chronic kidney disease. Advances in Chronic Kidney Disease, 12(4), 353–365. https://doi.org/10.1053/j.ackd.2005.07.011
Levin, A., Bakris, G. L., Molitch, M., Smulders, M., Tian, J., Williams, L., Andress, D., Duckworth, W., & Molitch, M. (2007). Prevalence of abnormal serum vitamin D, PTH, calcium, and phosphorus in patients with chronic kidney disease: Results of the study to evaluate early kidney disease. Kidney International, 71(1), 31–38. https://doi.org/10.1038/sj.ki.5002009
LaClair, R. E., Hellman, R. N., Karp, S. L., Kraus, M. A., Ofner, S. S., & Snowden, M. G. (2005). Prevalence of calcidiol deficiency in CKD: A cross-sectional study across latitudes in the United States. American Journal of Kidney Diseases, 45(6), 1026–1033. https://doi.org/10.1053/j.ajkd.2005.02.029
Teng, M., Wolf, M., Ofsthun, N. M., Lazarus, J. M., Herer, R., & Thadhani, R. (2005). Activated injectable vitamin D and hemodialysis survival: A historical cohort study. Journal of the American Society of Nephrology, 16(4), 1115–1125. https://doi.org/10.1681/ASN.2004070573
Agarwal, R., Acharya, M., Tian, J., Sinha, A., & Konishi, Y. (2005). Antiproteinuric effect of oral paricalcitol in chronic kidney disease. Kidney International, 68(6), 2823–
https://doi.org/10.1111/j.1523-1755.2005.00755.x
Teng, M., Wolf, M., Lowrie, E., & Thadhani, R. (2003). Survival of patients undergoing hemodialysis with paricalcitol or calcitriol therapy. The New England Journal of Medicine, 349(5), 446–456. https://doi.org/10.1056/NEJMoa022536
Wolf, M., & Thadhani, R. (2007). Vitamin D in patients with renal failure: A summary of observational mortality studies and steps moving forward. Journal of Steroid Biochemistry and Molecular Biology, 103(3–5), 487–490. https://doi.org/10.1016/j.jsbmb.2006.11.009
Shoben, A. B., Rudser, K. D., de Boer, I. H., Young, B., Kestenbaum, B., Roberts, W. L., & Stehman-Breen, C. (2008). Association of oral calcitriol with improved survival in nondialyzed CKD. Journal of the American Society of Nephrology, 19(9), 1613–1619. https://doi.org/10.1681/ASN.2007111164
Coen, G. (2008). Vitamin D: An old prohormone with an emergent role in chronic kidney disease. Journal of Nephrology, 21(3), 313–323.
Tan, X., Li, Y., & Liu, Y. (2006). Paricalcitol attenuates renal interstitial fibrosis in obstructive nephropathy. Journal of the American Society of Nephrology, 17(11), 3382–3393. https://doi.org/10.1681/ASN.2006050520
Kuhlmann, A., Haas, C. S., Gross, M. L., Lindenmeyer, M. T., & Gne, J. (2004). 1,25 Dihydroxyvitamin D₃ decreases podocyte loss and podocyte hypertrophy in the subtotally nephrectomized rat. American Journal of Physiology – Renal Physiology, 286(3), F526–F533.
https://doi.org/10.1152/ajprenal.00316.2003
Freundlich, M., Quiroz, Y., Zhang, Z., Wang, L., Cho, Y., & Brown, A. J. (2008). Suppression of renin–angiotensin gene expression in the kidney by paricalcitol. Kidney International, 74(9), 1394–1402. https://doi.org/10.1038/ki.2008.408
Mizobuchi, M., Morrissey, J., Finch, J. L., Martin, D. R., Slatopolsky, E., & London, R. R. (2007). Combination therapy with an angiotensin-converting enzyme inhibitor and a vitamin D analog suppresses the progression of renal insufficiency in uremic rats. Journal of the American Society of Nephrology, 18(7), 1796–1806. https://doi.org/10.1681/ASN.2006091028
Zhang, Z., Zhang, Y., Ning, G., & Zhang, Y. (2008). Combination therapy with AT₁ blocker and vitamin D analog markedly ameliorates diabetic nephropathy: Blockade of compensatory renin increase. Proceedings of the National Academy of Sciences of the United States of America, 105(43), 15896–15901. https://doi.org/10.1073/pnas.0803751105
Tan, X., Wen, X., & Liu, Y. (2008). Paricalcitol inhibits renal inflammation by promoting vitamin D receptor-mediated sequestration of NF κB signaling. Journal of the American Society of Nephrology, 19(10), 1741–1752. https://doi.org/10.1681/ASN.2007060666
Li, Y. C., Kong, J., Wei, M., Chen, Z. F., Liu, S. Q., Cao, L. P., & Zhang, W. J. (2002). 1,25 Dihydroxyvitamin D₃ is a negative endocrine regulator of the renin–angiotensin system. Journal of Clinical Investigation,
(2), 229–238. https://doi.org/10.1172/JCI15219
Andress, D. (2007). Nonclassical aspects of differential vitamin D receptor activation: Implications for survival in patients with chronic kidney disease. Drugs, 67(14), 1999–2012. https://doi.org/10.2165/00003495-200767140-00003
Sprague, S. M., Llach, F., Amdahl, M., Bamichas, G., Servilla, K., & Charytan, C. E. (2003). Paricalcitol versus calcitriol in the treatment of secondary hyperparathyroidism. Kidney International, 63(4), 1483–1490. https://doi.org/10.1046/j.1523-1755.2003.00878.x
Fryer, R. M., Rakestraw, P. A., Nakane, M., Wakefield, K. M., & Zhang, Y. (2007). Differential inhibition of renin mRNA expression by paricalcitol and calcitriol in C57BL/6 mice. Nephron Physiology, 106(2), 76–81. https://doi.org/10.1159/000104875
Mizobuchi, M., Finch, J. L., Martin, D. R., Li, R. X., Rogers, H. L., & London, R. R. (2007). Differential effects of vitamin D receptor activators on vascular calcification in uremic rats. Kidney International, 72(6), 709–715. https://doi.org/10.1038/sj.ki.5002406
Yoshino, J., Monkawa, T., Tsuji, M., Okubo, H., Goto, M., Kubo, T., & Hasegawa, K. (2007). Snail1 is
involved in the renal epithelial–mesenchymal transition. Biochemical
and Biophysical Research Communications, 362(1), 63–68. https://doi.org/10.1016/j.bbrc.2007.07.146
Boutet, A., De Frutos, C. A., Maxwell, P. H., Charnock-Jones, D. S., & Harris, A. L. (2006). Snail activation disrupts tissue homeostasis and induces fibrosis in the adult kidney.
The EMBO Journal, 25(23), 5603–5613. https://doi.org/10.1038/sj.emboj.7601421
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