scholarly journals Combined statin and angiotensin-converting enzyme (ACE) inhibitor treatment increases the lifespan of long-lived F1 male mice

AGE ◽  
2016 ◽  
Vol 38 (5-6) ◽  
pp. 379-391 ◽  
Author(s):  
Stephen R. Spindler ◽  
Patricia L. Mote ◽  
James M. Flegal
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Ace Inhibitor ◽  
Converting Enzyme ◽  
Male Mice ◽  
Inhibitor Treatment

Partial escape of angiotensin converting enzyme (ACE) inhibition during prolonged ACE inhibitor treatment

1992 ◽  
Vol 10 (8) ◽  
pp. 15 ◽  
Author(s):  
Anton H. van den Meiracker ◽  
Arie J. Man in??t Veld ◽  
Peter J.J. Admiraal ◽  
Henk J. Ritsema van Eck ◽  
Frans Boomsma ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Ace Inhibitor ◽  
Ace Inhibition ◽  
Converting Enzyme ◽  
Inhibitor Treatment

MicroRNAs mediate the cardioprotective effect of angiotensin-converting enzyme inhibition in acute kidney injury

2015 ◽  
Vol 309 (11) ◽  
pp. F943-F954 ◽  
Author(s):  
Indrajeetsinh Rana ◽  
Elena Velkoska ◽  
Sheila K. Patel ◽  
Louise M. Burrell ◽  
Fadi J. Charchar
Keyword(s):  
Kidney Disease ◽  
Angiotensin Converting Enzyme ◽  
Cardiac Hypertrophy ◽  
Inhibitory Action ◽  
Target Genes ◽  
Ace Inhibitor ◽  
Kidney Injury ◽  
Converting Enzyme ◽  
Subtotal Nephrectomy ◽  
Inhibitor Treatment

Cardiovascular disease, including cardiac hypertrophy, is common in patients with kidney disease and can be partially attenuated using blockers of the renin-angiotensin system (RAS). It is unknown whether cardiac microRNAs contribute to the pathogenesis of cardiac hypertrophy or to the protective effect of RAS blockade in kidney disease. Using a subtotal nephrectomy rat model of kidney injury, we investigated changes in cardiac microRNAs that are known to have direct target genes involved in the regulation of apoptosis, fibrosis, and hypertrophy. The effect of treatment with the angiotensin-converting enzyme (ACE) inhibitor ramipril on cardiac microRNAs was also investigated. Kidney injury led to a significant increase in cardiac microRNA-212 and microRNA-132 expression. Ramipril reduced cardiac hypertrophy, attenuated the increase in microRNA-212 and microRNA-132, and significantly increased microRNA-133 and microRNA-1 expression. There was altered expression of caspase-9, B cell lymphoma-2, transforming growth factor-β, fibronectin 1, collagen type 1A1, and forkhead box protein O3, which are all known to be involved in the regulation of apoptosis, fibrosis, and hypertrophy in cardiac cells while being targets for the above microRNAs. ACE inhibitor treatment increased expression of microRNA-133 and microRNA-1. The inhibitory action of ACE inhibitor treatment on increased cardiac NADPH oxidase isoform 1 expression after subtotal nephrectomy surgery suggests that inhibition of oxidative stress is also one of mechanism of ACE inhibitor-mediated cardioprotection. These finding suggests the involvement of microRNAs in the cardioprotective action of ACE inhibition in acute renal injury, which is mediated through an inhibitory action on profibrotic and proapoptotic target genes and stimulatory action on antihypertrophic and antiapoptotic target genes.

Tissue Expression of Components of the Renin—Angiotensin System in Experimental Post-Infarction Heart Failure in Rats: Effects of Heart Failure and Angiotensin-Converting Enzyme Inhibitor Treatment

1997 ◽  
Vol 92 (5) ◽  
pp. 455-465 ◽  
Author(s):  
Martin P. Kelly ◽  
OLE Kahr ◽  
Christian Aalkjaer ◽  
Frederic Cumin ◽  
Nilesh J Samani
Keyword(s):  
Heart Failure ◽  
Angiotensin Converting Enzyme ◽  
Ace Inhibitor ◽  
Mrna Level ◽  
Renin Angiotensin System ◽  
Mrna Levels ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Inhibitor Treatment

1. It has been suggested that local tissue renin—angiotensin systems may be activated in heart failure and that effects on such systems may, at least partially, explain the beneficial effects of angiotensin-converting enzyme (ACE) inhibitors in this syndrome. To investigate these hypotheses, we examined expression of renin-angiotensin system components in several tissues in a rodent model of post-myocardial infarction (MI) heart failure, and analysed whether such expression is modified by ACE inhibitor treatment. 2. Four groups of rats (n = 8–12 per group) were studied 30 days after surgery: (A) sham-operated rats with no treatment, (B) rats with post-MI heart failure induced by ligation of the left coronary artery, (C) sham-operated rats treated with the ACE inhibitor perindopril (1.5 mg day−1 kg−1), and (D) rats as per B, but treated with perindopril. Expression of renin, angiotensinogen, ACE and angiotensin subtype 1 receptor was assessed by quantification of their respective mRNAs by Northern blotting. 3. Renal renin mRNA increased 2-fold in animals with MI (group B) compared with controls (group A) (P < 0.05) and between 50 and 100-fold after ACE inhibitor treatment (P < 0.001). No change in renin gene expression was found in any extra-renal site either following MI or after ACE inhibitor treatment. Hepatic angiotensinogen mRNA level was similar in all groups, but kidney angiotensinogen mRNA level was increased 1.6-fold (P < 0.01) in the groups receiving perindopril. ACE mRNA level in the lung was not affected by ACE inhibitor treatment but decreased by 50% following MI (groups B and D, P < 0.01). This was associated with a similar (50%, P < 0.01) fall in lung ACE activity and was correlated with the severity of heart failure. Angiotensin subtype 1 receptor mRNA level was not affected in any tissue by either MI or ACE inhibitor treatment. 4. We did not find a systematic activation of tissue renin-angiotensin systems, as assessed by steady-state mRNA levels of key components of the system in experimental post-MI heart failure, or a major effect of ACE inhibitor treatment on expression of these components. However, we observed tissue-specific changes in expression of selected components of the renin-angiotensin system in the kidney and the lung in post-MI heart failure and after ACE inhibitor treatment, which may be of relevance to the pathophysiology of the syndrome and the effects of ACE inhibition.

scholarly journals The Level of hs-CRP in Coronary Artery Ectasia and Its Response to Statin and Angiotensin-Converting Enzyme Inhibitor Treatment

2007 ◽  
Vol 2007 ◽  
pp. 1-4 ◽  
Author(s):  
Yilmaz Ozbay ◽  
Mehmet Akbulut ◽  
Mehmet Balin ◽  
Hidayet Kayancicek ◽  
Adil Baydas ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Angiotensin Converting Enzyme ◽  
Ace Inhibitor ◽  
Enzyme Inhibitor ◽  
Inflammatory Marker ◽  
Converting Enzyme ◽  
Coronary Artery Ectasia ◽  
Increased Risk ◽  
Hs Crp ◽  
Inhibitor Treatment

Background/Aim. Coronary artery ectasia (CAE) was thought of as a variant of atherosclerosis. C-reactive protein (CRP) which is among the most sensitive markers of systemic inflammation, and elevation of systemic and local levels of this inflammatory marker which has been associated with an increased risk for cardiovascular disease in the obstructive coronary artery disease (O-CAD) are well known, but little was known in CAE. The anti-inflammatory effects of statins and the effect of angiotensin-converting enzyme (ACE) inhibitors on endothelial dysfunction are well established in atherosclerosis. The aim of the present study was to investigate CRP level and its response to statin and ACE inhibitor treatment in CAE.Materials and method. We measured serum hs-CRP level in 40 CAE (26 males, mean age:56.32±9years) and 41 O-CAD (34 males, mean age:57.19±10years) patients referred for elective coronary angiography at baseline and after 3-month statin and ACE inhibitor treatment.Results. Plasma hs-CRP levels were significantly higher in CAE group than O-CAD group at baseline (2.68±66mg/L versus1,64±64, resp.,P<.0001). Plasma hs-CRP levels significantly decreased from baseline 3 months later in the CE (from2.68±0.66mg/L to1.2±0.53mg/L,P<.0001) as well as in the O-CAD group (from1.64±0.64mg/L to1.01±0.56mg/L, P<.001).Conclusion. We think that hs-CRP measurement may be a good prognostic value in CAE patients as in stenotic ones. Further placebo-controlled studies are needed to evaluate the clinical significance of this decrease in hs-CRP.

scholarly journals A clinical dose of angiotensin-converting enzyme (ACE) inhibitor and heterozygous ACE deletion exacerbate Alzheimer's disease pathology in mice

2019 ◽  
Vol 294 (25) ◽  
pp. 9760-9770 ◽  
Author(s):  
Shuyu Liu ◽  
Fujiko Ando ◽  
Yu Fujita ◽  
Junjun Liu ◽  
Tomoji Maeda ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Angiotensin Converting Enzyme ◽  
Amyloid Precursor Protein ◽  
Ace Inhibitors ◽  
Ace Inhibitor ◽  
Precursor Protein ◽  
Causative Role ◽  
Converting Enzyme ◽  
Clinical Dose

Inhibition of angiotensin-converting enzyme (ACE) is a strategy used worldwide for managing hypertension. In addition to converting angiotensin I to angiotensin II, ACE also converts neurotoxic β-amyloid protein 42 (Aβ42) to Aβ40. Because of its neurotoxicity, Aβ42 is believed to play a causative role in the development of Alzheimer's disease (AD), whereas Aβ40 has neuroprotective effects against Aβ42 aggregation and also against metal-induced oxidative damage. Whether ACE inhibition enhances Aβ42 aggregation or impairs human cognitive ability are very important issues for preventing AD onset and for optimal hypertension management. In an 8-year longitudinal study, we found here that the mean intelligence quotient of male, but not female, hypertensive patients taking ACE inhibitors declined more rapidly than that of others taking no ACE inhibitors. Moreover, the sera of all AD patients exhibited a decrease in Aβ42-to-Aβ40–converting activity compared with sera from age-matched healthy individuals. Using human amyloid precursor protein transgenic mice, we found that a clinical dose of an ACE inhibitor was sufficient to increase brain amyloid deposition. We also generated human amyloid precursor protein/ACE+/− mice and found that a decrease in ACE levels promoted Aβ42 deposition and increased the number of apoptotic neurons. These results suggest that inhibition of ACE activity is a risk factor for impaired human cognition and for triggering AD onset.

Characterization of Angiotensin Converting Enzyme (ACE) in the Testis and Assessment of thein VivoEffects of the ACE Inhibitor Perindopril

Endocrinology ◽  
1988 ◽  
Vol 123 (1) ◽  
pp. 50-55 ◽  
Author(s):  
BRUCE JACKSON ◽  
ROSE B. CUBELA ◽  
KEIJI SAKAGUCHI ◽  
COLIN I. JOHNSTON
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Ace Inhibitor ◽  
Converting Enzyme

scholarly journals A systematic review and meta-analysis of angiotensin-converting enzyme inhibitor use and psoriasis incidence

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Gonjin Song ◽  
Ji Yea Kim ◽  
Ha Young Yoon ◽  
Jeong Yee ◽  
Hye Sun Gwak
Keyword(s):  
Systematic Review ◽  
Literature Review ◽  
Angiotensin Converting Enzyme ◽  
Subgroup Analysis ◽  
Ace Inhibitor ◽  
Web Of Science ◽  
Enzyme Inhibitor ◽  
Meta Analysis ◽  
Temperate Climate ◽  
Converting Enzyme

AbstractAlthough a considerable volume of data supporting induction or aggravation of psoriasis because of angiotensin-converting enzyme (ACE) inhibitor use exists, it remains insufficient for definitive conclusions. Therefore, we aimed to evaluate the association between ACE inhibitor use and psoriasis incidence through a systematic literature review and meta-analysis. We searched for qualifying studies across PubMed, Web of Science, and Embase. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to evaluate the strength of the association between ACE inhibitor use and psoriasis incidence. Eight studies with a total of 54,509 patients with a psoriasis diagnosis were included in this meta-analysis. The pooled OR for psoriasis incidence among ACE inhibitor users was 1.52 (95% CI, 1.16–2.00) compared to that among non-users. From subgroup analysis by continent, the OR for ACE inhibitor users versus non-users was 2.37 (95% CI 1.28–4.37) in Asia. Per the subgroup analysis by climate, the OR for ACE inhibitor users vs non-users in dry climate was 3.45 (95% CI: 2.05–5.79) vs 1.32 (95% CI 1.01–1.73) in temperate climate. Our results reveal a significant association between ACE inhibitor use and psoriasis incidence.

Sign in / Sign up

Export Citation Format

Share Document