Somatostatin antagonizes angiotensin II effects on mesangial cell contraction and glomerular filtration

This study examined interactions between adenosine (Ado) and angiotensin II (ANG II) in controlling renal blood flow (RBF) and glomerular filtration rate (GFR). In six normal dogs, intrarenal Ado infusion (1.0 mumol/min) transiently decreased RBF, but during sustained Ado infusion RBF increased to 122 +/- 7% of control, although GFR remained at 75 +/- 6% of control. Blockade of ANG II formation with the converting enzyme inhibitor SQ 14225 (n = 6) almost abolished the transient decrease in RBF but did not prevent the sustained fall in GFR caused by Ado. When circulating ANG II was held constant by intravenous infusion of SQ 14225 and 20 ng . kg-1 . min-1 of ANG II (n = 6), Ado transiently decreased RBF but the return of RBF was much slower than in normal dogs and RBF did not increase above control. Maintenance of constant circulating ANG II did not prevent Ado-mediated decreases in GFR. These observations suggest that Ado-mediated reductions in GFR do not depend entirely on ANG II and may be due to dilation of efferent arterioles by Ado. However, the transient renal vasoconstriction caused by Ado depends on ANG II, and data from this study suggest that part of the waning constrictor response to Ado is due to suppression of renin secretion and endogenous ANG II formation. In circumstances where high ANG II levels are maintained (i.e., ischemic renal failure), Ado may be capable of causing sustained renal vasoconstriction.

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Losartan prevents the mesangial cell‐myofibroblast transdifferentiation induced by high glucose and angiotensin II

The FASEB Journal ◽

10.1096/fasebj.24.1_supplement.812.7 ◽

2010 ◽

Vol 24 (S1) ◽

Author(s):

Carine Prisco Arnoni ◽

Edgar Maquigussa ◽

Luciana Guilhermino Pereira ◽

Mirian Aparecida Boim

Keyword(s):

Angiotensin Ii ◽

High Glucose ◽

Mesangial Cell

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Arachidonic Acid–Dependent Activation of a p22phox-Based NAD(P)H Oxidase Mediates Angiotensin II–Induced Mesangial Cell Protein Synthesis and Fibronectin Expression via Akt/PKB

Antioxidants and Redox Signaling ◽

10.1089/ars.2006.8.1497 ◽

2006 ◽

Vol 8 (9-10) ◽

pp. 1497-1508 ◽

Cited By ~ 31

Author(s):

Karen Block ◽

Jill M. Ricono ◽

Duck–Yoon Lee ◽

Basant Bhandari ◽

Goutam Ghosh Choudhury ◽

...

Keyword(s):

Protein Synthesis ◽

Arachidonic Acid ◽

Angiotensin Ii ◽

Mesangial Cell ◽

Cell Protein ◽

Fibronectin Expression

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Angiotensin II modulates the intrarenal effects of atrial natriuretic peptide

AJP Renal Physiology ◽

10.1152/ajprenal.1988.255.3.f545 ◽

1988 ◽

Vol 255 (3) ◽

pp. F545-F551

Author(s):

H. M. Siragy ◽

N. E. Lamb ◽

C. E. Rose ◽

M. J. Peach ◽

R. M. Carey

Keyword(s):

Glomerular Filtration Rate ◽

Angiotensin Ii ◽

Atrial Natriuretic Peptide ◽

Glomerular Filtration ◽

Plasma Flow ◽

Filtration Rate ◽

Renal Plasma Flow ◽

Systemic Effects ◽

Ang Ii ◽

Renal Effects

The mechanism by which atrial natriuretic peptide (ANP) increases renal water and solute excretion is not fully understood. We studied the renal effects of ANP and angiotensin II (ANG II) separately and together in uninephrectomized conscious dogs (n = 7) in sodium metabolic balance (80 meq/day). Exogenous ANG II and ANP were without measurable systemic effects as demonstrated by absence of changes in blood pressure, plasma aldosterone concentration, and plasma renin activity. The quantity of ANG II that had significant renal effects that were without measurable systemic effects was 0.2 pmol.kg-1.min-1. Three infusion rates of ANP had significant renal effects (1, 10, and 20 pmol.kg-1.min-1). These quantities of ANP caused significant diuresis, natriuresis, kaliuresis, and increased glomerular filtration rate without significant changes in renal plasma flow. ANG II alone caused significant antidiuresis, antinatriuresis, and decreased glomerular filtration rate and renal plasma flow. When ANG II and ANP were given together, no change in urinary flow rate, urinary sodium or potassium excretion, or renal plasma flow was observed, whereas glomerular filtration rate increased. Filtration fraction increased significantly with ANG II and ANP separately and together. Intrarenal ANP prevents the ANG II-induced decrement in urinary sodium excretion and urine flow rate. ANP may play an important role in escape from the sodium-retaining action of intrarenal ANG II.

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Sauchinone Protects Renal Mesangial Cell Dysfunction against Angiotensin II by Improving Renal Fibrosis and Inflammation

International Journal of Molecular Sciences ◽

10.3390/ijms21197003 ◽

2020 ◽

Vol 21 (19) ◽

pp. 7003

Author(s):

Jung Joo Yoon ◽

Hyeon Kyoung Lee ◽

Hye Yoom Kim ◽

Byung Hyuk Han ◽

Ho Sub Lee ◽

...

Keyword(s):

Cell Proliferation ◽

Diabetic Nephropathy ◽

Angiotensin Ii ◽

Mesangial Cell ◽

Mesangial Cells ◽

Tissue Growth ◽

Biologically Active ◽

Dependent Manner ◽

Saururus Chinensis ◽

Mesangial Cell Proliferation

Abnormal and excessive growth of mesangial cells is important in the pathophysiologic processes of diabetes-associated interstitial fibrosis and glomerulosclerosis, leading to diabetic nephropathy, which eventually turns into end-stage renal disease. Sauchinone, a biologically-active lignan isolated from aerial parts of Saururus chinensis, has anti-inflammatory and anti-viral activities effects on various cell types. However, there are no studies reporting the effects of sauchinone on diabetic nephropathy. The present study aims to investigate the role of sauchinone in mesangial cell proliferation and fibrosis induced by angiotensin II, as well as the underlying mechanisms of these processes. Human renal mesangial cells were induced by angiotensin II (AngII, 10 μM) in the presence or absence of sauchinone (0.1–1 μM) and incubated for 48 h. In this study, we found that AngII induced mesangial cell proliferation, while treatment with sauchinone inhibited the cell proliferation in a dose-dependent manner. Pre-treatment with sauchinone induced down-regulation of cyclins/CDKs and up-regulation of CDK inhibitor, p21, and p27kip1 expression. In addition, AngII-enhanced expression of fibrosis biomarkers such as fibronectin, collagen IV, and connective tissue growth factor (CTGF), which was markedly attenuated by sauchinone. Sauchinone also decreased AngII-induced TGF-β1 and Smad-2, Smad-3, and Smad-4 expression. This study further revealed that sauchinone ameliorated AngII-induced mesangial inflammation through disturbing activation of inflammatory factors, and NLRP3 inflammasome, which is composed of the NLRP3 protein, procaspase-1, and apoptosis-associated speck-like protein containing a CARD (ASC). Moreover, pretreatment of sauchinone inhibited NF-κB translocation and ROS production in AngII-exposed mesangial cells. These data suggest that sauchinone has a protective effect on renal proliferation, fibrosis and inflammation. Therefore, sauchinone might be a potential pharmacological agent in prevention of AngII-induced renal damage leading to diabetic nephropathy.

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Glomerular binding and contractile response to angiotensin II in rats with chronic experimental cirrhosis of the liver

Clinical Science ◽

10.1042/cs0800143 ◽

1991 ◽

Vol 80 (2) ◽

pp. 143-147 ◽

Cited By ~ 2

Author(s):

Luis M. Villamediana ◽

Mercedes Velo ◽

Ana Olivera ◽

Luis Hernando ◽

Carlos Caramelo ◽

...

Keyword(s):

Glomerular Filtration Rate ◽

Angiotensin Ii ◽

Glomerular Filtration ◽

Plasma Flow ◽

Filtration Rate ◽

Contractile Response ◽

Renal Plasma Flow ◽

Cross Sectional Area ◽

Sectional Area ◽

Cross Sectional

1. The effects of angiotensin II on glomerular filtration rate and renal plasma flow were studied in surgically instrumented conscious control and cirrhotic rats. In addition, angiotensin II binding and the contractile response to angiotensin II were studied in glomeruli isolated from cirrhotic and control rats. 2. Cirrhotic rats had a higher glomerular filtration rate and a higher renal plasma flow than control animals. A non-pressor dose of angiotensin II induced small but significant decreases in glomerular filtration rate and renal plasma flow in both control and cirrhotic rats, the effect on renal plasma flow being the most pronounced. 3. Plasma renin and aldosterone concentrations were similar in control and cirrhotic rats. 4. The cross-sectional area of glomeruli from cirrhotic rats was 42% greater than that of glomeruli from control animals. Angiotensin II (10−9 mol/l) decreased the cross-sectional area of glomeruli from control animals by 6.4 ± 0.9% and of glomeruli from cirrhotic rats by 6.6 ± 0.8% (P = not significant for comparison between control and cirrhotic animals). 5. There were no differences between control and cirrhotic rats in the affinity of angiotensin II for its glomerular receptors. However, the angiotensin II receptor density was higher in cirrhotic than in control rats, thereby producing an increased total angiotensin II binding in cirrhotic rats. 6. Since no functional differences between control and cirrhotic animals were present in the response to angiotensin II, even though angiotensin II binding was increased, a post-receptor blockade of the angiotensin II signal could be present in cirrhotic rats.

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