Pharmacokinetic/Pharmacodynamic Correlations of Selected Vasodilators
Hartmut Derendorf, Günther Hochhaus in Handbook of Pharmacokinetic/Pharmacodynamic Correlation, 2019
The usefulness of plasma renin or/and ACE activity in predicting the hypotensive effect of ACE inhibitors is still under debate. Johnston et al.30 reported a linear correlation between blood pressure reduction and inhibition in plasma ACE activity after administration of 10 mg of enalapril in hypertensive patients. Nilsen et al.31 found the correlation to be biphasic after administration of Cilazapril: the relationship between blood pressure and ACE inhibition was flat up to 90% ACE inhibition, whereas between 90 and 100% ACE inhibition the correlation was extremely steep, suggesting that more than 90% inhibition of plasma ACE was needed to obtain relevant blood pressure reductions. Despite these findings, it has been repeatedly demonstrated that plasma ACE activity did not correlate well with blood pressure reductions.32 For instance, several reports suggested a dissociation between plasma ACE activity and the fall in blood pressure after administration of Captopril,33 enalapril, and lisinopril.24 Individual enalapril plasma EC50 for the ACE inhibition also did not correlate with that for the blood pressure reduction.34 Dzau35 recently recommended the use of tissue (especially vascular) ACE activity for correlating hypotensive effects since it has been observed that tissue, not plasma, ACE concentrations correlated well with hypertensive events and with the duration of hypotensive response to ACE inhibitors in animal models.
Drug profiles: generic names A-Z
Jerome Z. Litt, Neil H. Shear in Litt's Drug Eruption & Reaction Manual, 2017
Clinically important, potentially hazardous interactions with: acebutolol, alfuzosin, captopril, cilazapril, diclofenac, enalapril, fosinopril, levodopa, levomepromazine, lisinopril, meloxicam, olmesartan, quinapril, ramipril, trandolapril, triamcinolone, trifluoperazine, zuclopenthixol
Development of UV–visible spectrophotometric methods for the quantitative and in silico studies for cilazapril optimized by response surface methodology
Published in Drug Development and Industrial Pharmacy, 2021
Drug determination is the basic step to monitor the remedial effects as discussed in book [1]. Spectroscopic methods, chiefly donor–acceptor based assays measures the effect of the drug on the acceptor species. For now, many diseases with idiosyncratic causes, USA based National Academy of Sciences has created the ‘New Taxonomy’ to elucidate diseases based on their causes along with symptoms. The subject of our study is (4S,7S)-7-[[(2S)-1-ethoxy-1-oxo-4-phenylbutan-2-yl]amino]-6-oxo-1,2,3,4,7,8,9,10-octahydropyridazino[1,2-a]diazepine-4-carboxylic acid (cilazapril; CLZ) which is an angiotensin-converting enzyme inhibitor used for the ameliorative cause for hypertension and congestive heart failure. Congestive heart failure is the dependent variable of hypertension out of three-quarters of all the reported cases. Cilazapril is officially listed in European Pharmacopoeia [2]. No document has been delivered till now regarding the degradation of the subject concerned according to WHO [3] and ICH [4]. However, humidity and temperature automated degradation have been described through autocatalytic reaction model [5]. Substantial literature based on the quantitative assay of the drug have been reported, but donor–acceptor phenomenon coupled with spectrophotometric determination sustains the larger part of research because of being cost-effective, rapid and sharp coloration, undemanding experimental setup [6].
Angiotensin converting enzyme and angiotensin converting enzyme inhibitors in dermatology: a narrative review
Published in Expert Review of Clinical Pharmacology, 2022
A literature search was conducted in PubMed, Embase and Google Scholar for relevant studies from 1985 to 5 July 2021 using the index words, ‘angiotensin converting enzyme inhibitors,’ ‘angiotensin II receptor blockers,’ ‘renin angiotensin system’ and the co-indexing terms ‘treatment,’ ‘captopril,’ ‘enalapril,’ ‘lisinopril,’ ‘ramipril,’ ‘perindopril,’ ‘trandolapril,’ ‘benazepril,’ ‘quinapril,’ ’fosinopril’, ‘imidapril,’ ‘zofenopril,’ ‘cilazapril,’ ‘moexipril,’ ‘cutaneous reaction’ and ‘dermatology.’ This review article was divided into three parts. The first part discusses the clinical use of ACEI in dermatology (Table 1, 2) (Figure 1). The second part describes the relationship between ACE and immune diseases, and further discusses the possible relationship between the clinical use of ACEI for these diseases and ACE (Table 3). The third part focuses on the cutaneous adverse reactions of ACEI.
Related Knowledge Centers
- Ace Inhibitor
- Stereoisomerism
- Hypertension
- Heart Failure
- Angiotensin-Converting Enzyme