The clinical use of angiotensin-converting enzyme inhibitors

Wong, J.; Patel, Ravindra P.; Kowey, Peter R.

doi:10.1016/j.pcad.2004.04.003

Cited by 87 publications

(55 citation statements)

References 52 publications

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“…These findings encouraged the search for orally active inhibitors of ACE; the first of these, captopril, was designed based on known inhibitors of another zinc-containing metalloprotease, carboxypeptidase A, and included a sulfhydryl-containing amino acid to serve as ligand for the zinc moiety. Because many of the side effects of captopril, such as proteinuria, skin rashes, and altered taste, were attributed to the sulfhydryl group, subsequent work led to the development of ACEIs that replaced this group with a carboxyl group (e.g., lisinopril, benazepril, quinapril, ramipril, perindopril, cilazapril, trandolapril) or phosphoryl group (fosinopril) [96,97]. The presence of the carboxyl group conferred greater lipophilicity, which actually improved binding to ACE, and improved tissue penetration [97].…”

Section: Main Characteristics Of Raas-suppressing Drugsmentioning

confidence: 99%

Effects of ACE-Inhibitors and Angiotensin Receptor Blockers on Inflammation

Raimondo¹,

Tuttolomondo²,

Buttà³

et al. 2012

CPD

112

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Abstract:The role of inflammation in cardiovascular disease and in hypertensive disease above all, is complex. Several studies confirm that activation of renin-angiotensin-aldosteron system (RAAS), through increase in the production of angiotensin II (Ang II), is closely related to local vascular inflammation. Over the BP lowering effects of anti-hypertensive treatments, several ancillary effects for every class may be found, distinguishing the various drugs from one another. Given the pro-inflammatory effects of Ang II and aldosterone, agents that interfere with the components of RAAS, such as ACE inhibitors, Angiotensin Recpetor Blockers (ARBs), and mineralocorticoid receptor antagonists (spironolactone or the more selective eplerenone), represent logical therapeutic tools to reduce vascular inflammation and cardiovascular risk, as suggested in large clinical trials in patients with hypertension and diabetes. Regarding ACE inhibitors, actually there is no convincing evidence indicating that ACEi's reduce plasma levels of major inflammatory markers in hypertension models. Lack of evidence concerns especially these inflammation markers, such as fibrinogen of CRP, which are less closely related to atherosclerotic disease and vascular damage and conversely are affected by several more aspecific factors. Results obtained by trials accomplished using ARBs seem to be more univocal to confirm, although to great extent, these is an anti-inflmmatory effect of drugs bocking AT1 receptor. In order to strictly study the effects of blockage of RAAS on inflammation, future studies may explore different strategies by, for example, simultaneously acting on the ACE and the AT1 angiotensin receptors.

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Section: Main Characteristics Of Raas-suppressing Drugsmentioning

confidence: 99%

Effects of ACE-Inhibitors and Angiotensin Receptor Blockers on Inflammation

Raimondo¹,

Tuttolomondo²,

Buttà³

et al. 2012

CPD

112

View full text Add to dashboard Cite

show abstract

“…Therefore, the efficacy of the combination of DRIs and ARBs might not be sufficiently evaluated. As ACE escape or angiotensin II production via non-ACE pathways could compromise the effect of ACEIs on the RAS, [40][41][42] the combination of DRIs and ARBs might be beneficial.…”

Section: Discussionmentioning

confidence: 99%

Aliskiren in combination with valsartan exerts synergistic protective effects against ventricular remodeling after myocardial infarction in mice

et al. 2011

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The efficacy of aliskiren, a direct renin inhibitor, in ventricular remodeling after myocardial infarction (MI) compared with conventional renin-angiotensin system (RAS) inhibitors remains to be defined. This study was performed to examine the protective effects of aliskiren and its addition to valsartan, an angiotensin-II receptor blocker, against ventricular remodeling after MI. MI was induced in 8-to 12-week-old C57BL/6 mice by ligating the left anterior descending artery. At 3 days after MI, mice were divided into five groups and were treated with the following: (1) phosphate-buffered saline (PBS); (2) hydralazine (10 mg kg -1 day -1 ); (3) valsartan (8 mg kg -1 day -1 ); (4) aliskiren (25 mg kg -1 day -1 ); and (5) combined aliskiren (25 mg kg -1 day -1 ) and valsartan (8 mg kg -1 day -1 ). With these doses of drugs, blood pressure-lowering effects compared with the PBS group were similar among the treated groups in sham-operated mice. At 28 days after MI, echocardiographic, hemodynamic and histological assessments demonstrated that monotherapy with valsartan or aliskiren alone significantly and similarly ameliorated ventricular remodeling after MI compared with the PBS and the hydralazine groups. Combination therapy of valsartan and aliskiren more greatly improved ventricular remodeling after MI with enhancement of angiogenesis and greater attenuation of tissue oxidative stress and inflammation. Our results indicate that aliskiren can be an alternative to conventional RAS inhibitors in the treatment of post-MI patients. Moreover, the dual therapy of valsartan and aliskiren may be more beneficial than either monotherapy. Further clinical trials will be warranted to sufficiently assess the safety and the efficacy of the use of aliskiren in post-MI patients.

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“…It is involved in the regulation of vascular resistance via converting angiotensin I to angiotensin II, the latter being a potent vasoconstrictor. A number of small molecule inhibitors targeting ACE such as lisinopril have been developed for the treatment of hypertension (24). Other than their applications in therapy, radiolabeled ACE inhibitors have been used for imaging and quantitative assessment of the ACE expression in the lungs (25)(26)(27).…”

Section: Surface Properties and Uptake Mechanisms Of Macromolecules Omentioning

confidence: 99%

Targeted Delivery of Nucleic Acid-Based Therapeutics to the Pulmonary Circulation

Kuruba

Wilson

Gao

et al. 2009

AAPS J

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Abstract. Targeted delivery of functional nucleic acids (genes and oligonucleotides) to pulmonary endothelium may become a novel therapy for the treatment of various types of lung diseases. It may also provide a new research tool to study the functions and regulation of novel genes in pulmonary endothelium. Its success is largely dependent on the development of a vehicle that is capable of efficient pulmonary delivery with minimal toxicity. This review summarizes the recent progress that has been made in our laboratory along these research directions. Factors that affect pulmonary nucleic acids delivery are also discussed.

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The clinical use of angiotensin-converting enzyme inhibitors

Cited by 87 publications

References 52 publications

Effects of ACE-Inhibitors and Angiotensin Receptor Blockers on Inflammation

Effects of ACE-Inhibitors and Angiotensin Receptor Blockers on Inflammation

Aliskiren in combination with valsartan exerts synergistic protective effects against ventricular remodeling after myocardial infarction in mice

Targeted Delivery of Nucleic Acid-Based Therapeutics to the Pulmonary Circulation

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