Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/9561
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dc.contributor.authorChai, Syn Yen
dc.contributor.authorPerich, Ren
dc.contributor.authorJackson, Ben
dc.contributor.authorMendelsohn, Frederick AOen
dc.contributor.authorJohnston, Colin Ien
dc.date.accessioned2015-05-15T22:42:24Z
dc.date.available2015-05-15T22:42:24Z
dc.date.issued1992-05-16en
dc.identifier.citationClinical and Experimental Pharmacology & Physiology. Supplement; 19(): 7-12en
dc.identifier.govdoc1327597en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/9561en
dc.description.abstract1. The effects of angiotensin-converting enzyme (ACE) inhibitors on the tissue ACE were assessed by quantitative in vitro autoradiography after acute and chronic administrations of the drugs. 2. Following acute administration of lisinopril, perindopril or benazepril, ACE was markedly inhibited in the lung, kidney and blood vessels but not in the testis. In the brain, ACE was inhibited mainly in structures with a deficient blood brain barrier. 3. High doses of perindopril progressively inhibited ACE in other brain structures. Tissue ACE inhibition persisted after serum levels of the enzyme had returned to control levels. In the case of perindopril, the time course of tissue ACE inhibition correlated with the inhibition of the pressor responses to exogenous angiotensin I. 4. After chronic administration of lisinopril or perindopril for 14 days, a similar pattern of ACE inhibition was observed in the kidney, lung and blood vessels. In the lung, however, lisinopril was found to increase total ACE by 30%, while plasma ACE was increased two-threefold by both lisinopril and perindopril. Testicular ACE remained unaltered by chronic lisinopril treatment. 5. Overall, the changes in tissue ACE after the administration of inhibitors more closely parallel the drugs' biological effects than changes in plasma ACE or drug levels. ACE in the testis and brain is protected by permeability barriers that limit access of the drugs.en
dc.language.isoenen
dc.subject.otherAdministration, Oralen
dc.subject.otherAngiotensin-Converting Enzyme Inhibitors.administration & dosage.pharmacologyen
dc.subject.otherAnimalsen
dc.subject.otherAutoradiographyen
dc.subject.otherBenzazepines.administration & dosage.pharmacokineticsen
dc.subject.otherBlood Vessels.enzymologyen
dc.subject.otherBlood-Brain Barrier.drug effectsen
dc.subject.otherBrain.enzymologyen
dc.subject.otherDipeptides.administration & dosage.pharmacologyen
dc.subject.otherIndoles.administration & dosage.pharmacokineticsen
dc.subject.otherKidney.enzymologyen
dc.subject.otherLisinoprilen
dc.subject.otherLung.enzymologyen
dc.subject.otherMaleen
dc.subject.otherPeptidyl-Dipeptidase A.blood.metabolismen
dc.subject.otherPerindoprilen
dc.subject.otherRatsen
dc.subject.otherRats, Sprague-Dawleyen
dc.subject.otherTime Factorsen
dc.titleAcute and chronic effects of angiotensin-converting enzyme inhibitors on tissue angiotensin-converting enzyme.en
dc.typeJournal Articleen
dc.identifier.journaltitleClinical and Experimental Pharmacology & Physiology. Supplementen
dc.identifier.affiliationUniversity of Melbourne Department of Medicine, Austin Hospital, Heidelberg, Victoria, Australiaen
dc.description.pages7-12en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/1327597en
dc.type.austinJournal Articleen
item.languageiso639-1en-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.openairetypeJournal Article-
item.grantfulltextnone-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
crisitem.author.deptGastroenterology and Hepatology-
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