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Angiotensin 2 type 1 receptor blockade different affects postishemic kidney injury in normotensive and hypertensive rats
Miloradović, Zoran; Ivanov, Milan; Jovović, Durdica; Karanović, Daniela; Vajić, Una Jovana; Marković-Lipkovski, Jasmina; Mihailović-Stanojević, Nevena; Milanović, Jelica Grujic.
Afiliação
  • Miloradović, Zoran; University of Belgrade. Institute for Medical Research. Belgrade. Serbia
  • Ivanov, Milan; University of Belgrade. Institute for Medical Research. Belgrade. Serbia
  • Jovović, Durdica; University of Belgrade. Institute for Medical Research. Belgrade. Serbia
  • Karanović, Daniela; University of Belgrade. Institute for Medical Research. Belgrade. Serbia
  • Vajić, Una Jovana; University of Belgrade. Institute for Medical Research. Belgrade. Serbia
  • Marković-Lipkovski, Jasmina; Medical School University of Belgrade. Institute of Pathology. Belgrade. Serbia
  • Mihailović-Stanojević, Nevena; University of Belgrade. Institute for Medical Research. Belgrade. Serbia
  • Milanović, Jelica Grujic; University of Belgrade. Institute for Medical Research. Belgrade. Serbia
J. physiol. biochem ; 72(4): 813-820, dic. 2016. graf, ilus
Artigo em Inglês | IBECS | ID: ibc-168386
Biblioteca responsável: ES1.1
Localização: BNCS
ABSTRACT
Many 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 (AU)
RESUMEN
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Assuntos
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Coleções: Bases de dados nacionais / Espanha Base de dados: IBECS Assunto principal: Traumatismo por Reperfusão / Losartan / Bloqueadores do Receptor Tipo 1 de Angiotensina II / Injúria Renal Aguda / Hipertensão / Rim Limite: Animais Idioma: Inglês Revista: J. physiol. biochem Ano de publicação: 2016 Tipo de documento: Artigo Instituição/País de afiliação: Medical School University of Belgrade/Serbia / University of Belgrade/Serbia
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Coleções: Bases de dados nacionais / Espanha Base de dados: IBECS Assunto principal: Traumatismo por Reperfusão / Losartan / Bloqueadores do Receptor Tipo 1 de Angiotensina II / Injúria Renal Aguda / Hipertensão / Rim Limite: Animais Idioma: Inglês Revista: J. physiol. biochem Ano de publicação: 2016 Tipo de documento: Artigo Instituição/País de afiliação: Medical School University of Belgrade/Serbia / University of Belgrade/Serbia
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