Involvement of proinflammatory cytokines in angiotensin II‑induced hypertension in rat

Maranduca,Minela   Aida; Tanase,Daniela   Maria; Branisteanu,Daniel   Constantin; Serban,Dragomir   Nicolae; Branisteanu,Daciana  Elena; Serban,Ionela   Lacramioara

doi:10.3892/etm.2020.9100

Involvement of proinflammatory cytokines in angiotensin II‑induced hypertension in rat

Authors:
- Minela Aida Maranduca
- Daniela Maria Tanase
- Daniel Constantin Branisteanu
- Dragomir Nicolae Serban
- Daciana Elena Branisteanu
- Ionela Lacramioara Serban
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Affiliations: Department of Physiology, ‘Grigore T. Popa’ University of Medicine and Pharmacy, 700115 Iasi, Romania, Department of Internal Medicine, ‘Grigore T. Popa’ University of Medicine and Pharmacy, 700115 Iasi, Romania, Department of Ophthalmology, ‘Grigore T. Popa’ University of Medicine and Pharmacy, 700115 Iasi, Romania, Department of Dermatology, ‘Grigore T. Popa’ University of Medicine and Pharmacy, 700115 Iasi, Romania
Published online on: August 5, 2020 https://doi.org/10.3892/etm.2020.9100
Pages: 3541-3545

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Abstract

Rightfully considered as essential for hydro‑electrolytic homeostasis, angiotensin II (Ang II) is the main product of the renin‑angiotensin system (RAS). Ang II is one of the most important factors that contribute to the regulation of systemic arterial blood pressure (ABP). This major role is based on the effects exerted by RAS: Upon the kidney (RAS involvement in the control of salt and water excretion), upon the brain (RAS involvement in the control of water intake), and upon the sympathetic nervous system. It is currently known that there is a tight bidirectional link between high ABP and chronic kidney disease (CKD). Ang II causes vasoconstriction in the renal microvasculature, predominantly in the preglomerular arterioles. High ABP affects the target organs (eyes, brain, heart, kidneys) and it is known both as a cause and as an effect of CKD. Thus, there is a positive feedback mechanism that contributes even more to the increase in ABP and the progression of CKD. Along with its main hemodynamic effects, Ang II has direct proinflammatory actions, that also affect the structure and function of the kidney and heart. This study investigated the role of RAS and Ang II in the inflammation that accompanies the hypertension experimentally induced by Ang II in rats. Our data support the hypothesis that anti‑inflammatory medication might alleviate the morphological and/or functional changes of the kidneys and heart that are related to Ang II‑induced hypertension.

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