scholarly journals P517Autocrine angiotensin II-signaling in FGF23-induced Ca2+-mediated hypertrophy in ventricular cardiomyocytes

2018 ◽  
Vol 114 (suppl_1) ◽  
pp. S126-S126
Author(s):  
K N Mhatre ◽  
P Wakula ◽  
E Bisping ◽  
B Pieske ◽  
F Heinzel
Keyword(s):  
Angiotensin Ii ◽  
Ventricular Cardiomyocytes ◽  
Angiotensin Ii Signaling

scholarly journals Disruption of angiotensin II signaling recouples eNOS in diabetes via dihydrofolate reductase

2006 ◽  
Vol 20 (4) ◽  
Author(s):  
Jeong‐Ho Oak ◽  
Karel Chalupsky ◽  
Hua “Linda” Cai
Keyword(s):  
Angiotensin Ii ◽  
Dihydrofolate Reductase ◽  
Angiotensin Ii Signaling

Local and Downstream Actions of Proximal Tubule Angiotensin II Signaling on Sodium Transporters in the Mouse Nephron

2021 ◽  
Author(s):  
Jonathan William Nelson ◽  
Alicia A. McDonough ◽  
Zhidan Xiang ◽  
Donna L. Ralph ◽  
Joshua A Robertson ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Proximal Tubule ◽  
Renin Angiotensin System ◽  
Cell Types ◽  
Sodium Reabsorption ◽  
Electrolyte Balance ◽  
Sodium Transporters ◽  
Lower Abundance ◽  
Angiotensin Ii Signaling ◽  
Distinct Cell

The renal nephron consists of a series of distinct cell types which function in concert to maintain fluid and electrolyte balance and blood pressure. The renin angiotensin system (RAS) is central to sodium and volume balance. We aimed to determine how loss of angiotensin II signaling in the proximal tubule (PT), which reabsorbs the bulk of filtered sodium and volume, impacts solute transport throughout the nephron. We hypothesized that proximal tubule (PT) RAS disruption would not only depress PT sodium transporters, but also impact downstream Na+ transporters. Utilizing a mouse model in which the type 1a angiotensin receptor (AT1aR) is deleted specifically within the PT (AT1aR PTKO), we profiled the abundance of sodium transporters, channels, and claudins along the nephron. Absence of PT AT1aR signaling was associated with lower abundance of PT transporters (NHE3, NBCe2 and claudin 2) as well as lower abundance of downstream transporters (total and phosphorylated NKCC2, medullary Na,K-ATPase, phosphorylated NCC and claudin 7) versus controls. However, transport activities of NKCC2 and NCC (assessed with diuretics) were similar between groups in order to maintain electrolyte balance. Together, these results demonstrate the primary impact of angiotensin II regulation on sodium reabsorption in PT at baseline and the associated influence on downstream Na+ transporters, highlighting the ability of the nephron to integrate sodium transport along the nephron to maintain homeostasis.

scholarly journals Angiotensin II Signaling in Vascular Smooth Muscle Cells Under High Glucose Conditions

Hypertension ◽  
1999 ◽  
Vol 33 (1) ◽  
pp. 378-384 ◽  
Author(s):  
Rama Natarajan ◽  
Stephen Scott ◽  
Wei Bai ◽  
Kiran Kumar V. Yerneni ◽  
Jerry Nadler
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
High Glucose ◽  
Muscle Cells ◽  
Angiotensin Ii Signaling

Angiotensin II stimulates apoptosis via TGF-β1 signaling in ventricular cardiomyocytes of rat

2006 ◽  
Vol 84 (11) ◽  
pp. 975-983 ◽  
Author(s):  
D. Schröder ◽  
J. Heger ◽  
H. M. Piper ◽  
G. Euler
Keyword(s):  
Angiotensin Ii ◽  
Ventricular Cardiomyocytes ◽  
Tgf Β1

scholarly journals Mechanisms of Increased Susceptibility to Angiotensin II–Induced Apoptosis in Ventricular Cardiomyocytes of Spontaneously Hypertensive Rats

Hypertension ◽  
2000 ◽  
Vol 36 (6) ◽  
pp. 1065-1071 ◽  
Author(s):  
Susana Ravassa ◽  
María Antonia Fortuño ◽  
Arantxa González ◽  
Begoña López ◽  
Guillermo Zalba ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Ventricular Cardiomyocytes ◽  
Induced Apoptosis ◽  
Increased Susceptibility
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