ACE2–angiotensin-(1–7)–Mas axis in renal ischaemia/reperfusion injury in rats

2010 ◽  
Vol 119 (9) ◽  
pp. 385-394 ◽  
Author(s):  
Kátia D. da Silveira ◽  
Kênia S. Pompermayer Bosco ◽  
Lúcio R. L. Diniz ◽  
Adriana K. Carmona ◽  
Giovanni D. Cassali ◽  
...  
Keyword(s):  
Kidney Injury ◽  
Renin Angiotensin System ◽  
At1 Receptor ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Ischaemia Reperfusion Injury ◽  
Mas Receptor ◽  
Angiotensin I Converting Enzyme ◽  
Ischaemia Reperfusion ◽  
Renal Expression

AngII (angiotensin II), ACE (angiotensin I-converting enzyme) and the AT1 receptor (AngII type 1 receptor) are associated with the inflammatory process and microvascular dysfunction of AKI (acute kidney injury) induced by renal I/R (ischaemia/reperfusion). However, Ang-(1–7) [angiotensin-(1–7)], ACE2 (angiotensin I-converting enzyme 2) and the Mas receptor also play a role in renal disease models. Therefore, in the present study, we have examined the renal profile of Ang-(1–7), ACE2 and the Mas receptor in renal I/R and compared them with that of AngII, ACE and the AT1 receptor. Male Wistar rats were submitted to left nephrectomy and ischaemia (45 min) followed by reperfusion (2 or 4 h) in the right kidney. At 4 h of reperfusion, renal AngII was increased (P<0.01) and renal Ang-(1–7) was decreased substantially (P<0.05), although plasma levels of both angiotensins were unchanged. In addition, renal I/R decreased the renal mRNA expression of renin (P<0.05), AT1 receptors (P<0.001) and ACE2 (P<0.05). At 2 and 4 h of reperfusion, renal ACE activity was reduced (P<0.05). On the other hand, renal expression of the Mas receptor was greatly increased at 4 h of reperfusion (P<0.01), which was confirmed by immunohistochemical and Western blot analysis. In conclusion, increased renal expression of the Mas receptor associated with changes in the RAS (renin–angiotensin system)-related peptidases support an important role for the ACE2–Ang-(1–7)–Mas axis in AKI.

scholarly journals Urinary angiotensinogen as a biomarker for acute to chronic kidney injury transition – prognostic and mechanistic implications

2018 ◽  
Vol 132 (21) ◽  
pp. 2383-2385 ◽  
Author(s):  
Katie L. Connor ◽  
Laura Denby
Keyword(s):  
Kidney Injury ◽  
Renin Angiotensin System ◽  
Ischaemia Reperfusion Injury ◽  
Angiotensin System ◽  
Urinary Angiotensinogen ◽  
Tubular Necrosis ◽  
Ischaemia Reperfusion ◽  
Structural Recovery ◽  
Chronic Kidney Injury ◽  
Injury Model

Accurate biomarkers that both predict the progression to, and detect the early stages of chronic kidney disease (CKD) are lacking, resulting in difficulty in identifying individuals who could potentially benefit from targeted intervention. In a recent issue [Clinical Science (2018) 132, 2121–2133], Cui et al. examine the ability of urinary angiotensinogen (uAGT) to predict the progression of acute kidney injury (AKI) to CKD. They principally employ a murine ischaemia reperfusion injury model to study this and provide data from a small prospective study of patients with biopsy proven acute tubular necrosis. The authors suggest that uAGT is a dynamic marker of renal injury that could be used to predict the likelihood of structural recovery following AKI. Here we comment on their findings, exploring the clinical utility of uAGT as a biomarker to predict AKI to CKD transition and perhaps more controversially, to discuss whether the early renin–angiotensin system blockade following AKI represents a therapeutic target.

scholarly journals Nandrolone increases angiotensin-I converting enzyme activity in rats tendons

2015 ◽  
Vol 21 (3) ◽  
pp. 173-177 ◽  
Author(s):  
Rita de Cassia Marqueti ◽  
Nara Yumi Hashimoto ◽  
João Luiz Quaglioti Durigan ◽  
Lívia Larissa Batista e Silva ◽  
Jeeser Alves de Almeida ◽  
...  
Keyword(s):  
Training Session ◽  
Renin Angiotensin System ◽  
Tissue Growth ◽  
Control Group ◽  
Activity Levels ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Angiotensin I Converting Enzyme ◽  
Tendon Adaptation ◽  
Ace Activity

INTRODUCTION: The renin-angiotensin system (RAS) has been associated with several biological processes of the human body, regulating, among others blood pressure and water and electrolytes balance. Moreover, RAS also regulates connective tissue growth. Recently, studies have shown that the use of nandrolone modifies the angiotensin-I converting enzyme (ACE) activity and increases collagen deposition in the heart. OBJECTIVE: The aim of study was to evaluate the Angiotensin-I converting enzyme (ACE) activity in the superficial flexor tendon (SFT) and in serum after load exercise in combination with anabolic androgenic steroid (AAS) administration after training session and six weeks of detraining. METHODS: Forty-eight Wistar rats were used into two groups (G1 and G2) subdivided into four subgroups: Sedentary (S); trained (T); AAS-treated (Deca-Durabolin(r), 5mg/kg, twice a week) sedentary rats (AAS) and AAS-treated and trained animals (AAST). Trained groups performed jumps in water: four series of 10 jumps each, followed by a 30 sec interval between the series, for seven weeks. RESULTS: Training increased ACE activity in the SFT compared to the control group (p <0.05). Both AAS and AAST groups presented higher ACE activity levels (p < 0.05). The AAST increased the ACE activity only compared to the trained animals. Only the AAST group presented significant higher levels of ACE in the serum. In the G2 group, all experimental groups presented decreased ACE activity in the serum and in the tendon, as compared to the control group. CONCLUSION: This study indicates that AAS administration and its combination with exercise increased ACE activity of tendons. AAS abuse could compromise tendon adaptation causing maladaptive remodeling.

Inhibition of angiotensin I–converting enzyme induces radioprotection by preserving murine hematopoietic short-term reconstituting cells

Blood ◽  
2004 ◽  
Vol 104 (4) ◽  
pp. 978-985 ◽  
Author(s):  
Sabine Charrier ◽  
Annie Michaud ◽  
Sabrina Badaoui ◽  
Sébastien Giroux ◽  
Eric Ezan ◽  
...  
Keyword(s):  
Ace Inhibitor ◽  
Plasma Concentrations ◽  
Ace Inhibition ◽  
At1 Receptor ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Short Term ◽  
Colony Forming Unit ◽  
Angiotensin I Converting Enzyme ◽  
Hematopoietic Toxicity

AbstractAngiotensin I–converting enzyme (ACE) inhibitors can affect hematopoiesis by several mechanisms including inhibition of angiotensin II formation and increasing plasma concentrations of AcSDKP (acetyl-N-Ser-Asp-Lys-Pro), an ACE substrate and a negative regulator of hematopoiesis. We tested whether ACE inhibition could decrease the hematopoietic toxicity of lethal or sublethal irradiation protocols. In all cases, short treatment with the ACE inhibitor perindopril protected against irradiation-induced death. ACE inhibition accelerated hematopoietic recovery and led to a significant increase in platelet and red cell counts. Pretreatment with perindopril increased bone marrow cellularity and the number of hematopoietic progenitors (granulocyte macrophage colony-forming unit [CFU-GM], erythroid burst-forming unit [BFU-E], and megakaryocyte colony-forming unit [CFU-MK]) from day 7 to 28 after irradiation. Perindopril also increased the number of hematopoietic stem cells with at least a short-term reconstitutive activity in animals that recovered from irradiation. To determine the mechanism of action involved, we evaluated the effects of increasing AcSDKP plasma concentrations and of an angiotensin II type 1 (AT1) receptor antagonist (telmisartan) on radioprotection. We found that the AT1-receptor antagonism mediated similar radioprotection as the ACE inhibitor. These results suggest that ACE inhibitors and AT1-receptor antagonists could be used to decrease the hematopoietic toxicity of irradiation.

scholarly journals Hypokalemia and Clinical Implications in Patients with Coronavirus Disease 2019 (COVID-19)

2020 ◽  
Author(s):  
Dong Chen ◽  
Xiaokun Li ◽  
Qifa Song ◽  
Chenchan Hu ◽  
Feifei Su ◽  
...  
Keyword(s):  
Gastrointestinal Symptoms ◽  
Renin Angiotensin System ◽  
Good Prognosis ◽  
Clinical Implications ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Angiotensin System ◽  
Angiotensin I Converting Enzyme ◽  
Underlying Causes ◽  
The Relationship

BACKGROUNDSARS-CoV-2 has caused a series of COVID-19 globally. SARS-CoV-2 binds angiotensin I converting enzyme 2 (ACE2) of renin–angiotensin system (RAS) and causes prevalent hypokalemiaMETHODSThe patients with COVID-19 were classified into severe hypokalemia, hypokalemia, and normokalemia group. The study aimed to determine the relationship between hypokalemia and clinical features, the underlying causes and clinical implications of hypokalemia.RESULTSBy Feb 15, 2020, 175 patients with COVID-19 (92 women and 83 men; median age, 46 [IQR, 34–54] years) were admitted to hospital in Wenzhou, China, consisting 39 severe hypokalemia-, 69 hypokalemia-, and 67 normokalemia patients. Gastrointestinal symptoms were not associated with hypokalemia among 108 hypokalemia patients (P > 0.05). Body temperature, CK, CK-MB, LDH, and CRP were significantly associated with the severity of hypokalemia (P<0.01). 93% of severe and critically ill patients had hypokalemia which was most common among elevated CK, CK-MB, LDH, and CRP. Urine K+ loss was the primary cause of hypokalemia. 1 severe hypokalemia patients was given 3 g/day, adding up to an average of 34 (SD=4) g potassium during hospital stay. The exciting finding was that patients responded well to K+ supplements when they were inclined to recovery.CONCLUSIONSHypokalemia is prevailing in patients with COVID-19. The correction of hypokalemia is challenging because of continuous renal K+ loss resulting from the degradation of ACE2. The end of urine K+ loss indicates a good prognosis and may be a reliable, in-time, and sensitive biomarker directly reflecting the end of adverse effect on RAS system.

scholarly journals Garlic Attenuates Plasma and Kidney ACE-1 and AngII Modulations in Early Streptozotocin-Induced Diabetic Rats: Renal Clearance and Blood Pressure Implications

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Khaled K. Al-Qattan ◽  
Martha Thomson ◽  
Divya Jayasree ◽  
Muslim Ali
Keyword(s):  
Blood Pressure ◽  
Renal Clearance ◽  
Renin Angiotensin System ◽  
Diabetic Rats ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Angiotensin System ◽  
Angiotensin I Converting Enzyme ◽  
Type 1 Dm

Raw garlic aqueous extract (GE) has ameliorative actions on the renin-angiotensin system in type-1 diabetes mellitus (DM); however its effects on plasma and kidney angiotensin I converting enzyme type-1 (ACE-1) and angiotensin II (AngII) require further elucidation. This study investigated the effect of GE on plasma and kidney ACE-1 and AngII concentrations and in relation to systemic and renal clearance indicators significant to blood pressure (BP) homeostasis in early streptozotocin- (STZ-) induced type-1 DM. Normal rats (n=10) received 0.5 mL normal saline (NR/NS), diabetic rats (n=10) received 0.5 mL NS (DR/NS), and treated diabetic rats (n=10) received 50 mg/0.1 mL/100 g body weight GE (DR/GE) as daily intraperitoneal injections for 8 weeks. Compared to NR/NS, DR/NS showed a significant increase in plasma ACE-1 and AngII and conversely a decrease in kidney ACE-1 and AngII. These changes were associated with an increase in BP and clearance functions. Alternatively and compared to DR/NS, DR/GE showed normalization or attenuation in plasma and kidney ACE-1 and AngII. These GE induced rectifications were associated with moderation in BP elevation and renal clearance functions. Garlic attenuates modulations in plasma and kidney ACE-1 and AngII, in addition to BP and renal clearance function in type-1 DM.

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