1. 1-(2-((1-(ethoxycarbonyl)-3-phenylpropyl)amino)-1-oxopropyl)octahydro-1h-indol-2-carboxylic Acid
2. Gopten
3. Mavik
4. Odrik
5. Ru 44570
6. Ru-44570
7. Ru44570
8. Udrik
1. 87679-37-6
2. Mavik
3. Gopten
4. Odrik
5. Trandolaprilum [latin]
6. Ru-44570
7. Ru 44570
8. (2s,3ar,7as)-1-[(2s)-2-[[(2s)-1-ethoxy-1-oxo-4-phenylbutan-2-yl]amino]propanoyl]-2,3,3a,4,5,6,7,7a-octahydroindole-2-carboxylic Acid
9. 1t0n3g9crc
10. Ru44570
11. Nsc-758939
12. (2s,3ar,7as)-1-((s)-n-((s)-1-carboxy-3-phenylpropyl)alanyl)hexahydro-2-indolinecarboxylic Acid, 1-ethyl Ester
13. Ncgc00182079-02
14. Trandolaprilum
15. Udrik
16. Dsstox_cid_3692
17. Dsstox_rid_77151
18. Dsstox_gsid_23692
19. Odric
20. Preran
21. (2s)-1-[(2r)-2-[[(2s)-1-ethoxy-1-oxo-4-phenylbutan-2-yl]amino]propanoyl]-2,3,3a,4,5,6,7,7a-octahydroindole-2-carboxylic Acid
22. Cas-87679-37-6
23. Ccris 6594
24. Mavik (tn)
25. Unii-1t0n3g9crc
26. Trandolapril [usp:inn:ban]
27. Ncgc00095153-01
28. Mfcd00865776
29. Trandolapril [mi]
30. Trandolapril [inn]
31. Trandolapril [jan]
32. Chembl1519
33. Trandolapril [vandf]
34. Schembl16610
35. Trandolapril [mart.]
36. Bidd:gt0804
37. Trandolapril [usp-rs]
38. Trandolapril [who-dd]
39. Trandolapril (jan/usp/inn)
40. Chebi:9649
41. Gtpl6453
42. Dtxsid2023692
43. Hsdb 8392
44. Hms3262j10
45. Trandolapril [orange Book]
46. Tarka Component Trandolapril
47. Trandolapril [ep Monograph]
48. Hy-b0592
49. Zinc1853205
50. Tox21_111453
51. Tox21_113152
52. Tox21_500924
53. Trandolapril [usp Monograph]
54. Bdbm50369775
55. S6468
56. Akos015843316
57. Akos015896050
58. Trandolapril Component Of Tarka
59. Ccg-222228
60. Db00519
61. Ks-1467
62. Lp00924
63. Nsc 758939
64. Sdccgsbi-0633768.p001
65. Ncgc00182079-03
66. Ncgc00261609-01
67. (2s,3ar,7as)-1-(((s)-1-ethoxy-1-oxo-4-phenylbutan-2-yl)-l-alanyl)octahydro-1h-indole-2-carboxylic Acid
68. (2s,3ar,7as)-1-(n-((1s)-1-((ethyloxy)carbonyl)-3-phenylpropyl)-l-alanyl)octahydro-1h-indole-2-carboxylic Acid
69. 1h-indole-2-carboxylic Acid, 1-((2s)-2-((1-(ethoxycarbonyl)-3-phenylpropyl)amino)-1-oxopropyl)octahydro-, (2s,3ar,7as)-
70. 1h-indole-2-carboxylic Acid, Octahydro-1-(2-((1-(ethoxycarbonyl)-3-phenylpropyl)amino)-1-oxopropyl)-, (2s-(1(r*(r*)),2-alpha,3a-alpha,7a-beta))-
71. Trandolapril, >=98% (hplc), White Powder
72. D00383
73. W18796
74. 679t376
75. A842336
76. Q929420
77. Sr-02000000917
78. Sr-02000000917-2
79. Brd-k28550399-001-01-4
80. Trandolapril, European Pharmacopoeia (ep) Reference Standard
81. Trandolapril, United States Pharmacopeia (usp) Reference Standard
82. (2s,3ar,7as)-1-[(2s)-2-[[(1s)-1-ethoxycarbonyl-3-phenyl-propyl]amino]propanoyl]-2,3,3a,4,5,6,7,7a-octahydroindole-2-carboxylic Acid
83. (2s,3ar,7as)-1-[(2s)-2-{[(2s)-1-ethoxy-1-oxo-4-phenylbutan-2-yl]amino}propanoyl]-octahydro-1h-indole-2-carboxylic Acid
84. 1h-indole-2-carboxylic Acid, Octahydro N-((2s)-1-ethoxy-1-oxo-4-phenylbutan-2-yl)-1-alanyl (2s,3ar,7as)
85. 2s,3ar,7as)-1-[(2s)-2-[[(1s)-1-(ethoxycarbonyl)-3-phenylpropyl]amino]-1-oxopropyl]octahydro-1h-indole-2-carboxylic Acid, Mavik
86. Trandolapril/(2s,3ar,7as)-1-[(2s)-2-[[(1s)-1-ethoxycarbonyl-3-phenyl-propyl]amino]propanoyl]-2,3,3a,4,5,6,7,7a-octahydroindole-2-carboxylicacid
| Molecular Weight | 430.5 g/mol |
|---|---|
| Molecular Formula | C24H34N2O5 |
| XLogP3 | 2 |
| Hydrogen Bond Donor Count | 2 |
| Hydrogen Bond Acceptor Count | 6 |
| Rotatable Bond Count | 10 |
| Exact Mass | 430.24677219 g/mol |
| Monoisotopic Mass | 430.24677219 g/mol |
| Topological Polar Surface Area | 95.9 Ų |
| Heavy Atom Count | 31 |
| Formal Charge | 0 |
| Complexity | 634 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 5 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
| 1 of 4 | |
|---|---|
| Drug Name | Mavik |
| PubMed Health | Trandolapril (By mouth) |
| Drug Classes | Antihypertensive, Cardiovascular Agent, Renal Protective Agent |
| Drug Label | Trandolapril is the ethyl ester prodrug of a nonsulfhydryl angiotensin converting enzyme (ACE) inhibitor, trandolaprilat. Trandolapril is chemically described as (2S, 3aR, 7aS)-1-[(S)-N-[(S)-1-Carboxy-3-phenylpropyl]alanyl] hexahydro-2-indolinecarbox... |
| Active Ingredient | Trandolapril |
| Dosage Form | Tablet |
| Route | Oral |
| Strength | 1mg; 4mg; 2mg |
| Market Status | Prescription |
| Company | Abbvie |
| 2 of 4 | |
|---|---|
| Drug Name | Trandolapril |
| PubMed Health | Trandolapril (By mouth) |
| Drug Classes | Antihypertensive, Cardiovascular Agent, Renal Protective Agent |
| Drug Label | Trandolapril is the ethyl ester prodrug of a nonsulfhydryl angiotensin converting enzyme (ACE) inhibitor, trandolaprilat. Trandolapril is chemically described as (2S,3aR,7aS)-1-[(S)-N-[(S)-1-Carboxy-3-phenylpropyl]alanyl] hexahydro-2-indolinecarboxyl... |
| Active Ingredient | Trandolapril |
| Dosage Form | Tablet |
| Route | Oral |
| Strength | 1mg; 4mg; 2mg |
| Market Status | Prescription |
| Company | Epic Pharma; Aurobindo Pharma; Lupin; Invagen Pharms; Watson Labs; Teva Pharms; Mylan |
| 3 of 4 | |
|---|---|
| Drug Name | Mavik |
| PubMed Health | Trandolapril (By mouth) |
| Drug Classes | Antihypertensive, Cardiovascular Agent, Renal Protective Agent |
| Drug Label | Trandolapril is the ethyl ester prodrug of a nonsulfhydryl angiotensin converting enzyme (ACE) inhibitor, trandolaprilat. Trandolapril is chemically described as (2S, 3aR, 7aS)-1-[(S)-N-[(S)-1-Carboxy-3-phenylpropyl]alanyl] hexahydro-2-indolinecarbox... |
| Active Ingredient | Trandolapril |
| Dosage Form | Tablet |
| Route | Oral |
| Strength | 1mg; 4mg; 2mg |
| Market Status | Prescription |
| Company | Abbvie |
| 4 of 4 | |
|---|---|
| Drug Name | Trandolapril |
| PubMed Health | Trandolapril (By mouth) |
| Drug Classes | Antihypertensive, Cardiovascular Agent, Renal Protective Agent |
| Drug Label | Trandolapril is the ethyl ester prodrug of a nonsulfhydryl angiotensin converting enzyme (ACE) inhibitor, trandolaprilat. Trandolapril is chemically described as (2S,3aR,7aS)-1-[(S)-N-[(S)-1-Carboxy-3-phenylpropyl]alanyl] hexahydro-2-indolinecarboxyl... |
| Active Ingredient | Trandolapril |
| Dosage Form | Tablet |
| Route | Oral |
| Strength | 1mg; 4mg; 2mg |
| Market Status | Prescription |
| Company | Epic Pharma; Aurobindo Pharma; Lupin; Invagen Pharms; Watson Labs; Teva Pharms; Mylan |
/CLINICAL TRIALS/ ClinicalTrials.gov is a registry and results database of publicly and privately supported clinical studies of human participants conducted around the world. The Web site is maintained by the National Library of Medicine (NLM) and the National Institutes of Health (NIH). Each ClinicalTrials.gov record presents summary information about a study protocol and includes the following: Disease or condition; Intervention (for example, the medical product, behavior, or procedure being studied); Title, description, and design of the study; Requirements for participation (eligibility criteria); Locations where the study is being conducted; Contact information for the study locations; and Links to relevant information on other health Web sites, such as NLM's MedlinePlus for patient health information and PubMed for citations and abstracts for scholarly articles in the field of medicine. Trandolapril is included in the database.
NIH/NLM; ClinicalTrials.Gov. Available from, as of August 30, 2017: https://clinicaltrials.gov/
Trandolapril tablets are indicated for the treatment of hypertension. It may be used alone or in combination with other antihypertensive medication such as hydrochlorothiazide. /Included in US product label/
NIH; DailyMed. Current Medication Information for Trandolapril Tablets (Updated: July 2017). Available from, as of November 9, 2017: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=10f25119-9970-46fe-bf36-6fec6064895b
Trandolapril tablets are indicated in stable patients who have evidence of left-ventricular systolic dysfunction (identified by wall motion abnormalities) or who are symptomatic from congestive heart failure within the first few days after sustaining acute myocardial infarction. Administration of trandolapril to Caucasian patients has been shown to decrease the risk of death (principally cardiovascular death) and to decrease the risk of heart failure-related hospitalization. /Included in US product label/
NIH; DailyMed. Current Medication Information for Trandolapril Tablets (Updated: July 2017). Available from, as of November 9, 2017: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=10f25119-9970-46fe-bf36-6fec6064895b
ACE inhibitors have been used in the management of heart failure, usually in conjunction with other agents such as cardiac glycosides, diuretics, and beta-blockers. /Angiotensin-converting enzyme (ACE) inhibitors; NOT included in US product label/
American Society of Health-System Pharmacists 2017; Drug Information 2017. Bethesda, MD. 2017
For more Therapeutic Uses (Complete) data for Trandolapril (6 total), please visit the HSDB record page.
/BOXED WARNING/ When pregnancy is detected, discontinue trandolapril as soon as possible. Drugs that act directly on the renin-angiotensin system can cause injury and death to the developing fetus.
NIH; DailyMed. Current Medication Information for Trandolapril Tablets (Updated: July 2017). Available from, as of November 9, 2017: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=10f25119-9970-46fe-bf36-6fec6064895b
Angioedema of the face, extremities, lips, tongue, glottis, and larynx has been reported in patients treated with angiotensin-converting enzyme (ACE) inhibitors including trandolapril. Symptoms suggestive of angioedema or facial edema occurred in 0.13% of trandolapril-treated patients. Two of the four cases were life-threatening and resolved without treatment or with medication (corticosteroids). Angioedema associated with laryngeal edema can be fatal. If laryngeal stridor or angioedema of the face, tongue or glottis occurs, treatment with trandolapril should be discontinued immediately, the patient treated in accordance with accepted medical care and carefully observed until the swelling disappears. In instances where swelling is confined to the face and lips, the condition generally resolves without treatment; antihistamines may be useful in relieving symptoms.
NIH; DailyMed. Current Medication Information for Trandolapril Tablets (Updated: July 2017). Available from, as of November 9, 2017: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=10f25119-9970-46fe-bf36-6fec6064895b
Use of drugs that act on the renin-angiotensin system during the second and third trimesters of pregnancy reduces fetal renal function and increases fetal and neonatal morbidity and death. Resulting oligohydramnios can be associated with fetal lung hypoplasia and skeletal deformations. Potential neonatal adverse effects include skull hypoplasia, anuria, hypotension, renal failure, and death. When pregnancy is detected, discontinue trandolapril as soon as possible. These adverse outcomes are usually associated with use of these drugs in the second and third trimester of pregnancy. Most epidemiologic studies examining fetal abnormalities after exposure to antihypertensive use in the first trimester have not distinguished drugs affecting the renin-angiotensin system from other antihypertensive agents. Appropriate management of maternal hypertension during pregnancy is important to optimize outcomes for both mother and fetus. /Angiotensin-converting enzyme (ACE) inhibitors/
NIH; DailyMed. Current Medication Information for Trandolapril Tablets (Updated: July 2017). Available from, as of November 9, 2017: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=10f25119-9970-46fe-bf36-6fec6064895b
Like other angiotensin-converting enzyme (ACE) inhibitors, trandolapril rarely is associated with hypotension in patients with uncomplicated hypertension. Symptomatic hypotension may occur; patients at particular risk include those with severe volume and/or salt depletion secondary to prolonged diuretic therapy, dietary salt restriction, dialysis, diarrhea, or vomiting. Volume and/or salt depletion should be corrected before starting trandolapril therapy. Marked hypotension, which may be associated with oliguria and/or progressive azotemia and rarely with acute renal failure and/or death, may occur in patients with heart failure (with or without associated renal impairment). In patients with heart failure, trandolapril therapy should be started at the recommended dose under close medical supervision with close monitoring for the first 2 weeks of treatment and whenever the dosage of trandolapril or diuretic is increased. Hypotension also should be avoided in patients with ischemic heart disease, aortic stenosis, or cerebrovascular disease.
American Society of Health-System Pharmacists 2017; Drug Information 2017. Bethesda, MD. 2017
For more Drug Warnings (Complete) data for Trandolapril (13 total), please visit the HSDB record page.
For the treatment of mild to moderate hypertension, as an adjunct in the treatment of congestive heart failure (CHF), to improve survival following myocardial infarction (MI) in individuals who are hemodynamically stable and demonstrate symptoms of left ventricular systolic dysfunction or signs of CHF within a few days following acute MI, and to slow progression of renal disease in hypertensive patients with diabetes mellitus and microalbuminuria or overt nephropathy.
Treatment of hypertension
Trandolapril is the ethyl ester prodrug of a nonsulfhydryl ACE inhibitor, trandolaprilat. Trandolapril is deesterified in the liver to the diacid metabolite, trandolaprilat, which is approximately eight times more active as an inhibitor of ACE than its parent compound. ACE is a peptidyl dipeptidase that is part of the RAAS. The RAAS is a homeostatic mechanism for regulating hemodynamics, water and electrolyte balance. During sympathetic stimulation or when renal blood pressure or blood flow is reduced, renin is released from the granular cells of the juxtaglomerular apparatus in the kidneys. In the blood stream, renin cleaves circulating angiotensinogen to ATI, which is subsequently cleaved to ATII by ACE. ATII increases blood pressure via a number of mechanisms. First, it stimulates the secretion of aldosterone from the adrenal cortex. Aldosterone travels to the distal convoluted tubule (DCT) and collecting tubule of nephrons where it increases sodium and water reabsorption by increasing the number of sodium channels and sodium-potassium ATPases on cell membranes. Second, ATII stimulates the secretion of vasopressin (also known as antidiuretic hormone or ADH) from the posterior pituitary gland. ADH stimulates further water reabsorption from the kidneys via insertion of aquaporin-2 channels on the apical surface of cells of the DCT and collecting tubules. Third, ATII increases blood pressure through direct arterial vasoconstriction. Stimulation of the Type 1 ATII receptor on vascular smooth muscle cells leads to a cascade of events resulting in myocyte contraction and vasoconstriction. In addition to these major effects, ATII induces the thirst response via stimulation of hypothalamic neurons. ACE inhibitors inhibit the rapid conversion of ATI to ATII and antagonize RAAS-induced increases in blood pressure. ACE (also known as kininase II) is also involved in the enzymatic deactivation of bradykinin, a vasodilator. Inhibiting the deactivation of bradykinin increases bradykinin levels and may further sustain the effects of trandolaprilat by causing increased vasodilation and decreased blood pressure. The blood pressure lowering effect of trandolaprilat is due to a decrease in peripheral vascular resistance, which is not accompanied by significant changes in urinary excretion of chloride or potassium or water or sodium retention.
Angiotensin-Converting Enzyme Inhibitors
A class of drugs whose main indications are the treatment of hypertension and heart failure. They exert their hemodynamic effect mainly by inhibiting the renin-angiotensin system. They also modulate sympathetic nervous system activity and increase prostaglandin synthesis. They cause mainly vasodilation and mild natriuresis without affecting heart rate and contractility. (See all compounds classified as Angiotensin-Converting Enzyme Inhibitors.)
Antihypertensive Agents
Drugs used in the treatment of acute or chronic vascular HYPERTENSION regardless of pharmacological mechanism. Among the antihypertensive agents are DIURETICS; (especially DIURETICS, THIAZIDE); ADRENERGIC BETA-ANTAGONISTS; ADRENERGIC ALPHA-ANTAGONISTS; ANGIOTENSIN-CONVERTING ENZYME INHIBITORS; CALCIUM CHANNEL BLOCKERS; GANGLIONIC BLOCKERS; and VASODILATOR AGENTS. (See all compounds classified as Antihypertensive Agents.)
C - Cardiovascular system
C09 - Agents acting on the renin-angiotensin system
C09A - Ace inhibitors, plain
C09AA - Ace inhibitors, plain
C09AA10 - Trandolapril
Absorption
~ 40-60% absorbed; extensive first pass metabolism results in a low bioavailability of 4-14%
Route of Elimination
After oral administration of trandolapril, about 33% of parent drug and metabolites are recovered in urine, mostly as trandolaprilat, with about 66% in feces.
Volume of Distribution
18 L
Clearance
52 L/h [After approximately 2 mg IV doses]
/MILK/ Trandolapril and its metabolites are distributed into milk in rats.
American Society of Health-System Pharmacists 2017; Drug Information 2017. Bethesda, MD. 2017
After oral administration of trandolapril, about 33% of parent drug and metabolites are recovered in urine, mostly as trandolaprilat, with about 66% in feces. The extent of the absorbed dose which is biliary excreted has not been determined. Plasma concentrations (Cmax and AUC of trandolapril and Cmax of trandolaprilat) are dose proportional over the 1-4 mg range, but the AUC of trandolaprilat is somewhat less than dose proportional. In addition to trandolaprilat, at least 7 other metabolites have been found, principally glucuronides or deesterification products.
NIH; DailyMed. Current Medication Information for Trandolapril Tablets (Updated: July 2017). Available from, as of November 9, 2017: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=10f25119-9970-46fe-bf36-6fec6064895b
Serum protein binding of trandolapril is about 80%, and is independent of concentration. Binding of trandolaprilat is concentration-dependent, varying from 65% at 1000 ng/mL to 94% at 0.1 ng/mL, indicating saturation of binding with increasing concentration.
NIH; DailyMed. Current Medication Information for Trandolapril Tablets (Updated: July 2017). Available from, as of November 9, 2017: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=10f25119-9970-46fe-bf36-6fec6064895b
Absolute bioavailability after oral administration of trandolapril is about 10% as trandolapril and 70% as trandolaprilat. After oral trandolapril under fasting conditions, peak trandolapril levels occur at about one hour and peak trandolaprilat levels occur between 4 and 10 hours. The elimination half-life of trandolapril is about 6 hours. At steady state, the effective half-life of trandolaprilat is 22.5 hours. Like all ACE inhibitors, trandolaprilat also has a prolonged terminal elimination phase, involving a small fraction of administered drug, probably representing binding to plasma and tissue ACE. During multiple dosing of trandolapril, there is no significant accumulation of trandolaprilat. Food slows absorption of trandolapril, but does not affect AUC or Cmax of trandolaprilat or Cmax of trandolapril.
NIH; DailyMed. Current Medication Information for Trandolapril Tablets (Updated: July 2017). Available from, as of November 9, 2017: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=10f25119-9970-46fe-bf36-6fec6064895b
The volume of distribution of trandolapril is about 18 liters. Total plasma clearances of trandolapril and trandolaprilat after approximately 2 mg IV doses are about 52 liters/hour and 7 liters/hour respectively. Renal clearance of trandolaprilat varies from 1- 4 liters/hour, depending on dose.
NIH; DailyMed. Current Medication Information for Trandolapril Tablets (Updated: July 2017). Available from, as of November 9, 2017: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=10f25119-9970-46fe-bf36-6fec6064895b
Cleavage of the ester group of trandolapril, primarily in the liver, is responsible for conversion to trandolaprilat, the active metabolite. Seven other metabolites, including diketopiperazine and glucuronide conjugated derivatives of trandolapril and trandolaprilat, have been identified.
Trandolapril is a prodrug and has little pharmacologic activity until hydrolyzed in the liver to trandolaprilat.
American Society of Health-System Pharmacists 2017; Drug Information 2017. Bethesda, MD. 2017
Trandolapril's angiotensin-converting enzyme (ACE)-inhibiting activity is primarily due to its diacid metabolite, trandolaprilat. Cleavage of the ester group of trandolapril, primarily in the liver, is responsible for conversion.
NIH; DailyMed. Current Medication Information for Trandolapril Tablets (Updated: July 2017). Available from, as of November 9, 2017: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=10f25119-9970-46fe-bf36-6fec6064895b
After oral administration of trandolapril, about 33% of parent drug and metabolites are recovered in urine, mostly as trandolaprilat, with about 66% in feces. ... In addition to trandolaprilat, at least 7 other metabolites have been found, principally glucuronides or deesterification products.
NIH; DailyMed. Current Medication Information for Trandolapril Tablets (Updated: July 2017). Available from, as of November 9, 2017: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=10f25119-9970-46fe-bf36-6fec6064895b
The elimination half lives of trandolapril and trandolaprilat are about 6 and 10 hours, respectively, but, similar to all ACE inhibitors, trandolaprilat also has a prolonged terminal elimination phase that involves a small fraction of administered drug. This likely represents drug binding to plasma and tissue ACE. The effective half life of elimination for trandolaprilat is 16-24 hours.
At steady state, the effective half-life of trandolaprilat is 22.5 hours. /Trandolaprilat/
NIH; DailyMed. Current Medication Information for Trandolapril Tablets (Updated: July 2017). Available from, as of November 9, 2017: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=10f25119-9970-46fe-bf36-6fec6064895b
There are two isoforms of ACE: the somatic isoform, which exists as a glycoprotein comprised of a single polypeptide chain of 1277; and the testicular isoform, which has a lower molecular mass and is thought to play a role in sperm maturation and binding of sperm to the oviduct epithelium. Somatic ACE has two functionally active domains, N and C, which arise from tandem gene duplication. Although the two domains have high sequence similarity, they play distinct physiological roles. The C-domain is predominantly involved in blood pressure regulation while the N-domain plays a role in hematopoietic stem cell differentiation and proliferation. ACE inhibitors bind to and inhibit the activity of both domains, but have much greater affinity for and inhibitory activity against the C-domain. Trandolaprilat, the active metabolite of trandolapril, competes with ATI for binding to ACE and inhibits and enzymatic proteolysis of ATI to ATII. Decreasing ATII levels in the body decreases blood pressure by inhibiting the pressor effects of ATII as described in the Pharmacology section above. Trandolaprilat also causes an increase in plasma renin activity likely due to a loss of feedback inhibition mediated by ATII on the release of renin and/or stimulation of reflex mechanisms via baroreceptors.
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