Angiotensin 2 type 1 receptor blockade different affects postishemic kidney injury in normotensive and hypertensive rats
Само за регистроване кориснике
2016
Аутори
Miloradović, ZoranIvanov, Milan
Jovović, Đurđica
Karanović, Danijela
Vajić, Una Jovana
Marković-Lipkovski, Jasmina
Mihailović-Stanojević, Nevena
Grujić-Milanović, Jelica
Чланак у часопису (Објављена верзија)
Метаподаци
Приказ свих података о документуАпстракт
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 associa...ted 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.
Кључне речи:
Postishemic kidney injury / Losartan / Normotension / Hypertension / ExperimentalИзвор:
Journal of Physiology & Biochemistry, 2016, 72, 4, 813-820Издавач:
- Springer, Dordrecht
Финансирање / пројекти:
DOI: 10.1007/s13105-016-0514-4
ISSN: 1138-7548
PubMed: 27534651
WoS: 000388101700021
Scopus: 2-s2.0-84982279846
Институција/група
Institut za medicinska istraživanjaTY - JOUR AU - Miloradović, Zoran AU - Ivanov, Milan AU - Jovović, Đurđica AU - Karanović, Danijela AU - Vajić, Una Jovana AU - Marković-Lipkovski, Jasmina AU - Mihailović-Stanojević, Nevena AU - Grujić-Milanović, Jelica PY - 2016 UR - http://rimi.imi.bg.ac.rs/handle/123456789/682 AB - 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. PB - Springer, Dordrecht T2 - Journal of Physiology & Biochemistry T1 - Angiotensin 2 type 1 receptor blockade different affects postishemic kidney injury in normotensive and hypertensive rats EP - 820 IS - 4 SP - 813 VL - 72 DO - 10.1007/s13105-016-0514-4 ER -
@article{ author = "Miloradović, Zoran and Ivanov, Milan and Jovović, Đurđica and Karanović, Danijela and Vajić, Una Jovana and Marković-Lipkovski, Jasmina and Mihailović-Stanojević, Nevena and Grujić-Milanović, Jelica", year = "2016", 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.", publisher = "Springer, Dordrecht", journal = "Journal of Physiology & Biochemistry", title = "Angiotensin 2 type 1 receptor blockade different affects postishemic kidney injury in normotensive and hypertensive rats", pages = "820-813", number = "4", volume = "72", doi = "10.1007/s13105-016-0514-4" }
Miloradović, Z., Ivanov, M., Jovović, Đ., Karanović, D., Vajić, U. J., Marković-Lipkovski, J., Mihailović-Stanojević, N.,& Grujić-Milanović, J.. (2016). Angiotensin 2 type 1 receptor blockade different affects postishemic kidney injury in normotensive and hypertensive rats. in Journal of Physiology & Biochemistry Springer, Dordrecht., 72(4), 813-820. https://doi.org/10.1007/s13105-016-0514-4
Miloradović Z, Ivanov M, Jovović Đ, Karanović D, Vajić UJ, Marković-Lipkovski J, Mihailović-Stanojević N, Grujić-Milanović J. Angiotensin 2 type 1 receptor blockade different affects postishemic kidney injury in normotensive and hypertensive rats. in Journal of Physiology & Biochemistry. 2016;72(4):813-820. doi:10.1007/s13105-016-0514-4 .
Miloradović, Zoran, Ivanov, Milan, Jovović, Đurđica, Karanović, Danijela, Vajić, Una Jovana, Marković-Lipkovski, Jasmina, Mihailović-Stanojević, Nevena, Grujić-Milanović, Jelica, "Angiotensin 2 type 1 receptor blockade different affects postishemic kidney injury in normotensive and hypertensive rats" in Journal of Physiology & Biochemistry, 72, no. 4 (2016):813-820, https://doi.org/10.1007/s13105-016-0514-4 . .