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dc.creatorMiloradović, Zoran
dc.creatorIvanov, Milan
dc.creatorJovović, Đurđica
dc.creatorKaranović, Danijela
dc.creatorVajić, Una Jovana
dc.creatorMarković-Lipkovski, Jasmina
dc.creatorMihailović-Stanojević, Nevena
dc.creatorGrujić-Milanović, Jelica
dc.date.accessioned2021-04-20T12:46:16Z
dc.date.available2021-04-20T12:46:16Z
dc.date.issued2016
dc.identifier.issn1138-7548
dc.identifier.urihttp://rimi.imi.bg.ac.rs/handle/123456789/682
dc.description.abstractMany studies demonstrated that angiotensin 2 type 1 receptor (AT1R) blockade accelerates renal recovery in post-ischaemic kidney but there are many controversies related to its net effect on kidney structure and function. During the past years, our research group was trying to define the pathophysiological significance of the renin-angiotensin system on post-ischemic acute renal failure (ARF) development in normotensive Wistar as well as hypertensive rats (SHR). This review mostly summarizes our experience in that field. Our previous studies in normotensive rats revealed that AT1R blockade, except slightly renal vascular resistance improvement, had no other obvious beneficial effects, and therefore implies angiotensin 2 (Ang-2) overexpression as non-dominant on kidney reperfusion injuries development. Similarly it was observed in Wistar rats with induced mild (L-NAME, 3 mg/kg b.w.) nitric oxide (NO) deficiency. Expectably, in strong induced (L-NAME, 10 mg/kg b.w.) NO deficiency associated with ARF, massive tubular injuries indicate harmful effects of AT1R blockade, implying strongly disturbed glomerular filtration and suggesting special precaution related to AT1R blockers usage. Opposite to previous, by our opinion, AT1R antagonism promises new advance in treatment of essentially hypertensive subjects who develop ARF. Increased glomerular filtration, diminished oxidative stress, and most importantly improved tubular structure in postishemic SHR treated with AT1R blocker losartan, implicate Ang-2 over production as potently agent in the kidney ischemic injury, partly trough generation of reactive oxygen species. These data contribute understanding the pathogenesis of this devastating illness in hypertensive surroundings.en
dc.publisherSpringer, Dordrecht
dc.relationinfo:eu-repo/grantAgreement/MESTD/Basic Research (BR or ON)/175096/RS//
dc.rightsrestrictedAccess
dc.sourceJournal of Physiology & Biochemistry
dc.subjectPostishemic kidney injuryen
dc.subjectLosartanen
dc.subjectNormotensionen
dc.subjectHypertensionen
dc.subjectExperimentalen
dc.titleAngiotensin 2 type 1 receptor blockade different affects postishemic kidney injury in normotensive and hypertensive ratsen
dc.typearticle
dc.rights.licenseARR
dc.citation.epage820
dc.citation.issue4
dc.citation.other72(4): 813-820
dc.citation.rankM22
dc.citation.spage813
dc.citation.volume72
dc.identifier.doi10.1007/s13105-016-0514-4
dc.identifier.pmid27534651
dc.identifier.scopus2-s2.0-84982279846
dc.identifier.wos000388101700021
dc.type.versionpublishedVersion


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Приказ основних података о документу