The Relationship between the Adrenal Tissue Renin-Angiotensin System, Internalization of the Type I Angiotensin II Receptor (AT1) and Angiotensin II Function in the Rat Adrenal Zona Glomerulosa Cell

1995 ◽  
pp. 319-329 ◽  
Author(s):  
G. P. Vinson ◽  
M. M. Ho ◽  
J. R. Puddefoot ◽  
R. Teja ◽  
S. Barker ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Zona Glomerulosa ◽  
Type I ◽  
Angiotensin Ii Receptor ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Adrenal Tissue ◽  
The Relationship

Localization of angiotensin II receptor and local renin-angiotensin system in human colonic mucosa

2001 ◽  
Vol 120 (5) ◽  
pp. A313-A314
Author(s):  
Koki Hirasawa ◽  
Yoshihiko Sato ◽  
Yoshisuke Hosoda ◽  
Tatsuo Yamamoto ◽  
Hiroyuki Hanai
Keyword(s):  
Angiotensin Ii ◽  
Colonic Mucosa ◽  
Renin Angiotensin System ◽  
Angiotensin Ii Receptor ◽  
Angiotensin System ◽  
Renin Angiotensin

Role of adrenal renin-angiotensin system in the control of aldosterone secretion in sodium-restricted rats

2000 ◽  
Vol 278 (6) ◽  
pp. E1027-E1030 ◽  
Author(s):  
Giuseppina Mazzocchi ◽  
Ludwik K. Malendowicz ◽  
Anna Markowska ◽  
Giovanna Albertin ◽  
Gastone G. Nussdorfer
Keyword(s):  
Enzyme Inhibitor ◽  
Renin Angiotensin System ◽  
Zona Glomerulosa ◽  
Normal Diet ◽  
Angiotensin Ii Receptor ◽  
Aldosterone Secretion ◽  
Angiotensin System ◽  
Renin Angiotensin

This study examined the effect of the pharmacological manipulation of adrenal renin-angiotensin system (RAS) on aldosterone secretion from in situ perfused adrenals of rats kept on a normal diet and sodium restricted for 14 days. Neither the angiotensin-converting enzyme inhibitor captopril nor the nonselective angiotensin II receptor antagonist saralasin and the AT1 receptor-selective antagonist losartan affected basal aldosterone output in normally fed rats. In contrast, they concentration dependently decreased aldosterone secretion in sodium-restricted animals, with maximal effective concentration ranging from 10− 7 to 10− 6 M. Captopril (10− 6 M), saralasin (10− 6 M), and losartan (10− 7 M) counteracted aldosterone response to 10 mM K+ in sodium-restricted rats but not in normally fed animals. Collectively, these findings provide evidence that adrenal RAS plays a role in the regulation of aldosterone secretion, but only under conditions of prolonged stimulation of zona glomerulosa probably leading to overexpression of adrenal RAS.

Role of the renin-angiotensin system in the pathogenesis of preeclampsia

2005 ◽  
Vol 288 (4) ◽  
pp. F614-F625 ◽  
Author(s):  
Dinesh M. Shah
Keyword(s):  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Receptor Activation ◽  
Gravid Uterus ◽  
Type I ◽  
Hypertensive Disorder ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Organ Systems

Preeclampsia is a hypertensive disorder unique to pregnancy with consistent involvement of the kidney. The renin-angiotensin system (RAS) has been implicated in the pathogenesis of preeclampsia. In the gravid state, in addition to the RAS in the kidney, there is a tissue-based RAS in the uteroplacental unit. Increased renin expression observed both in human preeclampsia and in a transgenic mouse model with a human preeclampsia-like syndrome supports the concept that activation of the uteroplacental RAS, with angiotensin II entering the systemic circulation, may mediate the pathogenesis of preeclampsia. A novel disease paradigm of the two-kidney one-clip (2K-1C) Goldblatt model is presented for preeclampsia, wherein the gravid uterus is the clipped “kidney” and the two maternal kidneys represent the unclipped kidney. Validation of the 2K-1C Goldblatt model analogy requires evidence of elevated angiotensin II in the peripheral circulation before vascular maladaptation in preeclampsia. Convincing evidence of the elevation of angiotensin II in preeclampsia does not exist despite the fact that much of vascular pathogenesis appears to be due to angiotensin type I (AT1) receptor activation. Vascular maladaptation with increased vasomotor tone, endothelial dysfunction, and increased sensitivity to angiotensin II and norepinephrine in manifest preeclampsia may be explained on the basis of angiotensin II-mediated mechanisms. Recently, novel angiotensin II-related biomolecular mechanisms have been described in preeclampsia. These include AT1and bradykinin B2receptor heterodimerization and the production of an autoantibody against AT1. Various organ systems with a predilection for involvement in preeclampsia are each a site of a tissue-based RAS. How angiotensin II-mediated mechanisms may explain the primary clinical-pathological features of preeclampsia is described. Future investigations are proposed to more precisely define the role of activation of the uteroplacental RAS in the mechanisms underlying preeclampsia.

scholarly journals The Renin-Angiotensin System: A Key Role in SARS-CoV-2- Induced COVID-19

Molecules ◽  
2021 ◽  
Vol 26 (22) ◽  
pp. 6945
Author(s):  
George El-Arif ◽  
Antonella Farhat ◽  
Shaymaa Khazaal ◽  
Cédric Annweiler ◽  
Hervé Kovacic ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Organ Damage ◽  
World Health ◽  
Electrolyte Balance ◽  
Type I ◽  
Related Factors ◽  
Angiotensin System ◽  
Mortality And Morbidity ◽  
Renin Angiotensin

The novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19), was first identified in Eastern Asia (Wuhan, China) in December 2019. The virus then spread to Europe and across all continents where it has led to higher mortality and morbidity, and was declared as a pandemic by the World Health Organization (WHO) in March 2020. Recently, different vaccines have been produced and seem to be more or less effective in protecting from COVID-19. The renin–angiotensin system (RAS), an essential enzymatic cascade involved in maintaining blood pressure and electrolyte balance, is involved in the pathogenicity of COVID-19, since the angiotensin-converting enzyme II (ACE2) acts as the cellular receptor for SARS-CoV-2 in many human tissues and organs. In fact, the viral entrance promotes a downregulation of ACE2 followed by RAS balance dysregulation and an overactivation of the angiotensin II (Ang II)–angiotensin II type I receptor (AT1R) axis, which is characterized by a strong vasoconstriction and the induction of the profibrotic, proapoptotic and proinflammatory signalizations in the lungs and other organs. This mechanism features a massive cytokine storm, hypercoagulation, an acute respiratory distress syndrome (ARDS) and subsequent multiple organ damage. While all individuals are vulnerable to SARS-CoV-2, the disease outcome and severity differ among people and countries and depend on a dual interaction between the virus and the affected host. Many studies have already pointed out the importance of host genetic polymorphisms (especially in the RAS) as well as other related factors such age, gender, lifestyle and habits and underlying pathologies or comorbidities (diabetes and cardiovascular diseases) that could render individuals at higher risk of infection and pathogenicity. In this review, we explore the correlation between all these risk factors as well as how and why they could account for severe post-COVID-19 complications.

scholarly journals Liver Protective Effects of Renin-Angiotensin System Inhibition Have No Survival Benefits in Hepatocellular Carcinoma Induced By Repetitive Administration of Diethylnitrosamine in Mice

2018 ◽  
Vol 6 (6) ◽  
pp. 955-960 ◽  
Author(s):  
Sameh Saber ◽  
Amr Mahmoud ◽  
Noha Helal ◽  
Eman El-Ahwany ◽  
Rasha Abdelghany
Keyword(s):  
Hepatocellular Carcinoma ◽  
Overall Survival ◽  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Rank Test ◽  
Protective Effects ◽  
Angiotensin Ii Receptor ◽  
Converting Enzyme Inhibitors ◽  
Angiotensin System ◽  
Renin Angiotensin

BACKGROUND: Preclinical studies have demonstrated that renin-angiotensin system (RAS) signalling has strong tumour-promoting effects and RAS inhibition was associated with improvement in the overall survival in some cancer types including hepatocellular carcinoma (HCC).OBJECTIVE: We aimed to investigate the effect of angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin-II-receptor blockers (ARBs) on the survival of mice with diethylnitrosamine (DEN) induced HCC.METHODS: HCC was induced by weekly i.p. administration of DEN. Mice were treated with sorafenib (SO) (30 mg/kg), perindopril (PE) (1 mg/kg), fosinopril (FO) (2 mg/kg), losartan (LO) (10 mg/kg), PE (1 mg/kg) + SO (30 mg/kg), FO (2 mg/kg) + SO (30 mg/kg), or LO (10 mg/kg) + SO (30 mg/kg). Survival analysis was done using the Kaplan-Meier method, and the log-rank test was used for assessing the significance of difference between groups.RESULTS: The administration of PE, FO and LO as monotherapy or as combined with SO resulted in marked improvement in the liver histologic picture with no impact on overall survival of mice.CONCLUSION: Interfering the RAS either through the inhibition of ACE or the blockade of angiotensin II type 1 (AT1) receptors has similar effects on the liver of DEN-induced HCC mice and is not associated with longer survival due to detrimental effects of DEN on other organs. Hence, repetitive administration of DEN in such models of HCC is not suitable for mortality assessment studies.

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