Приказ основних података о документу

dc.creatorJerkić, Mirjana
dc.creatorVaragić, Jasmina
dc.creatorJovović, D.
dc.creatorRadujković-Kuburović, Gordana
dc.creatorNastic-Mirić, D
dc.creatorAdanja-Grujić, G
dc.creatorMarković-Lipkovski, Jasmina
dc.creatorDimitrijević, J
dc.creatorMiloradović, Zoran
dc.creatorVojvodić, SB
dc.date.accessioned2021-04-20T12:04:58Z
dc.date.available2021-04-20T12:04:58Z
dc.date.issued1999
dc.identifier.issn0931-0509
dc.identifier.urihttp://rimi.imi.bg.ac.rs/handle/123456789/53
dc.description.abstractBackground. The pathophysiology of renal ischaemia, resulting in tubular cell injury and leading to acute renal failure (ARF), remains unclear. An ever-increasing number of investigations focus on a possible role of nitric oxide (NO) in regulating circulation during ARF. In this context, we investigated the influence of chronic stimulation or inhibition of NO synthesis, or both, on haemodynamic parameters, histology and plasma renin activity (PRA) after ischaemia-reperfusion injury of rat kidneys. Methods, Experiments were performed on adult, male Wistar rats. Before induction of ARF, a group of animals was treated with a NO synthesis inhibitor (L-NAME) and another group was treated with a precursor of NO synthesis (L-arginine). The animals received those substances for 4 weeks. Control groups received the same amount of tap water for 4 or 8 weeks and were divided into groups with ARF (4 weeks-ARF group and 8 weeks-ARF group) and a sham-operated group. Another group of rats was treated first with L-NAME and then with L-arginine in their drinking water, for 4 weeks for each of these two substances. All parameters were evaluated 24 h after the induction of ischaemic ARF or the sham operation. Results, Our results show that such long-term stimulation of NO release by L-arginine improved renal haemodynamics in the ischaemic form of ARF. Renal blood Bow (RBF) increased by 96% in the L-arginine-treated rats with ARF compared with the group with ARF alone. Inhibition of NO synthesis worsens renal haemodynamics after ARF. However, this aggravation can be reversed by L-arginine. The rate of water reabsorption was reduced in all groups with ARF, but this reduction was least in the group treated with L-arginine. The rate of Na+ reabsorption was reduced in all groups 24 h after renal ischaemia, but a significant decrease was observed after the inhibition of NO synthesis. Histological examination of the kidney specimens showed that morphological changes were least in the rats treated with L-arginine, when compared with all other groups with ARF. Nevertheless, the lesions were most prominent in the L-NAME + ARF group. In this group, the areas of corticomedullar necrosis were more widespread in comparison with other groups, especially the L-arginine group where only swelling of the proximal tubular cells was observed. Treatment with L-NAME was not accompanied by any significant alteration in the plasma concentration of angiotensin I (ANG I), while in the group treated with L-arginine ANG I had a tendency to decrease. Conclusions. Acute post-ischaemic renal failure may be alleviated by administering the NO substrate (L-arginine). NO acts cytoprotectively on tubular epithelial cells in ischaemia-reperfusion injury of rat kidney. Evidence of this comes from both histopathological findings and increased tubular water and sodium reabsorption. However, inhibition of NO synthesis (provoked by L-NAME) worsens renal haemodynamics and aggravates morphological changes after ARF. These aggravations can, however, be reversed by L-arginine.en
dc.publisherOxford Univ Press, Oxford
dc.rightsopenAccess
dc.sourceNephrology Dialysis Transplantation
dc.subjectacute renal failureen
dc.subjectangiotensin Ien
dc.subjecthaemodynamicsen
dc.subjectnitric oxideen
dc.subjectrenal morphologyen
dc.titleL-arginine reduces tubular cell injury in acute post-ischaemic renal failureen
dc.typearticle
dc.rights.licenseARR
dc.citation.epage1407
dc.citation.issue6
dc.citation.other14(6): 1398-1407
dc.citation.rankM22
dc.citation.spage1398
dc.citation.volume14
dc.identifier.doi10.1093/ndt/14.6.1398
dc.identifier.fulltexthttp://rimi.imi.bg.ac.rs/bitstream/id/391/50.pdf
dc.identifier.pmid10382999
dc.identifier.scopus2-s2.0-0032972513
dc.identifier.wos000080623200010
dc.type.versionpublishedVersion


Документи

Thumbnail

Овај документ се појављује у следећим колекцијама

Приказ основних података о документу