Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.15.1 (ACE)
 18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of the renin-angiotensin system on renal hemodynamics, tubular pressure and tubulo-glomerular feedback was investigated with the angiotensin converting enzyme inhibitor MK 421 (enalapril), in uninephrectomized rats with and without ischemia-induced acute renal failure. In animals with normal renal function proximal tubular pressure and tubulo-glomerular feedback response were lowered by enalapril long-term treatment, whereas glomerular filtration rate and renal blood flow were not influenced by the drug. After 45 and 70 minutes ischemia there was no difference between treated and untreated animals in the severely impaired glomerular filtration rate. Renal blood flow remained unaffected by the treatment. The histological damage due to ischemia (tubular casts, tubular necrosis and medullary capillary congestion) was not influenced by enalapril. As tubulo-glomerular feedback had been significantly inhibited during renin-angiotensin inhibition, its importance in mediating acute renal failure remains doubtful; other factors such as tubular obstruction and medullary congestion may be crucial.
 ...
PMID:The angiotensin converting enzyme inhibitor enalapril in acute ischemic renal failure in rats. 283 Oct 78

The present study was designed to investigate the effect of captopril, a sulfhydryl (-SH) containing ACE inhibitor and lisinopril, a non-SH containing ACE inhibitor, on ischaemia-reperfusion-induced renal injury in rats and to study the involvement of the free radical scavenging property of captopril in its renoprotective effect. Bilateral renal artery occlusion was induced for 30 min followed by reperfusion for 24 h. Blood samples were taken from retro orbital sinus before surgery and at 24 h after reperfusion for blood urea and blood creatinine estimation. After completion of 24 h of renal reperfusion the carotid artery was cannulated and the mean arterial blood pressure (MABP) was recorded. The left kidney was used for histological examination. The right kidney was utilised for estimation of mitochondrial thiobarbituric acid reactive substances (TBARS). Renal ischaemia, followed by reperfusion, significantly increased blood urea nitrogen (BUN) and blood creatinine. However, creatinine clearance decreased markedly. Captopril administered before renal artery occlusion or immediately after reperfusion and lisinopril pre-treatment significantly attenuated the increase in BUN and blood creatinine. Creatinine clearance was markedly better in captopril-treated animals as compared to lisinopril-treated rats. Captopril significantly decreased the degree of tubular necrosis, haemorrhagic streaks and urinary casts. Lisinopril treatment decreased tubular necrosis and urinary casts but no marked effect on haemorrhagic streaks was noted. Administration of captopril before ischaemia or just after reperfusion significantly reduced the elevated concentration of mitochondrial TBARS but no such decrease was noted in lisinopril-treated rats. Based on these results it may be concluded that captopril and lisinopril markedly protected against ischaemia-reperfusion-induced renal injury and any additional renoprotective effect of captopril may be ascribed to its free radical scavenging properties.
 ...
PMID:Effect of angiotensin converting enzyme inhibitors on ischaemia-reperfusion-induced renal injury in rats. 950 76

All types of acute kidney injury (AKI) (functional /pre-renal, parenchymal/intra-renal, obstructive/post-renal) result in a sharp drop of the glomerular filtration rate, with variable reversibility according to the initial cause. In one case out of five, drug intake can be related to the onset of AKI. Antibiotics, analgesics and nonsteroidal anti-inflammatory drugs, angiotensin converting enzyme inhibitors and angiotensin II receptor antagonists are the agents mostly involved, as well as iodinated radio-contrast agents. Mechanisms are often complex: toxic cellular effect directed on a nephron segment (tubular necrosis) associated or not with intraglomerular hemodynamic changes, or immune process leading to acute tubule-interstitial nephritis. Each underlying risk factor (age > 60 year, cardiac or hepatic failure, hypertension, diabetes, intra-vascular volume depletion, preexisting or unknown chronic kidney disease) must be taken into consideration by the prescribing physician because it reduces the chance of functional recovery and worsens the renal and the overall prognosis. A pre-renal additional component is often present and avoidable thanks to a strict hemodynamic monitoring. The present article summarizes some recent physiopathological aspects of AKI and makes the link between clinical situations and currently prescribed drugs. Lessons from the radio-contrast induced nephropathy are examined by taking into account prevention aspects and risk factors screening. An effective collaboration between the general practitioner and the nephrologist would benefit in optimizing the treatment of difficult cases.
 ...
PMID:[Acute kidney injury and drug-induced nephropathies]. 2203 61