scholarly journals SP166ADENOSINE A2 RECEPTORS ARE INDISPENSABLE FOR THE MAINTANANCE OF RENAL BLOOD FLOW UNDER ACUTE ISCHEMIA

2017 ◽  
Vol 32 (suppl_3) ◽  
pp. iii159-iii160
Author(s):  
Kentaro Fujii ◽  
Kazutoshi Miyashita ◽  
Akiko Kubo ◽  
Masaaki Sato ◽  
Aika Hagiwara ◽  
...  
2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Shiro Ono ◽  
Hideto Matsui ◽  
Masashi Noda ◽  
Shogo Kasuda ◽  
Noritaka Yada ◽  
...  

Abstract Acute kidney injury (AKI), an abrupt loss of renal function, is often seen in clinical settings and may become fatal. In addition to its hemostatic functions, von Willebrand factor (VWF) is known to play a role in cross-talk between inflammation and thrombosis. We hypothesized that VWF may be involved in the pathophysiology of AKI, major causes of which include insufficient renal circulation or inflammatory cell infiltration in the kidney. To test this hypothesis, we studied the role of VWF in AKI using a mouse model of acute ischemia-reperfusion (I/R) kidney injury. We analyzed renal function and blood flow in VWF-gene deleted (knock-out; KO) mice. The functional regulation of VWF by ADAMTS13 or a function-blocking anti-VWF antibody was also evaluated in this pathological condition. Greater renal blood flow and lower serum creatinine were observed after reperfusion in VWF-KO mice compared with wild-type (WT) mice. Histological analysis also revealed a significantly lower degree of tubular damage and neutrophil infiltration in kidney tissues of VWF-KO mice. Both human recombinant ADAMTS13 and a function-blocking anti-VWF antibody significantly improved renal blood flow, renal function and histological findings in WT mice. Our results indicate that VWF plays a role in the pathogenesis of AKI. Proper functional regulation of VWF may improve the microcirculation and vessel function in the kidney, suggesting a novel therapeutic option against AKI.


1978 ◽  
Vol 38 (5) ◽  
pp. 495-499 ◽  
Author(s):  
Torbjörn Leivestad ◽  
Erling Brodwall ◽  
Svein Simonsen

1990 ◽  
Vol 31 (5) ◽  
pp. 538-539
Author(s):  
G. M. Cleator ◽  
P. E. Klapper ◽  
A. G. Lewis ◽  
H. L. Sharma ◽  
A. M. Smith

Author(s):  
Bashair A. Alhummiany ◽  
David Shelley ◽  
Margaret Saysell ◽  
Maria‐Alexandra Olaru ◽  
Bernd Kühn ◽  
...  

2000 ◽  
Vol 279 (4) ◽  
pp. R1268-R1276 ◽  
Author(s):  
Paul P. Leyssac ◽  
Niels-Henrik Holstein-Rathlou ◽  
Ole Skøtt

Inconsistencies in previous reports regarding changes in early distal NaCl concentration (EDNaCl) and renin secretion during osmotic diuresis motivated our reinvestigation. After intravenous infusion of 10% mannitol, EDNaCl fell from 42.6 to 34.2 mM. Proximal tubular pressure increased by 12.6 mmHg. Urine flow increased 10-fold, and sodium excretion increased by 177%. Plasma renin concentration (PRC) increased by 58%. Renal blood flow and glomerular filtration rate decreased, however end-proximal flow remained unchanged. After a similar volume of hypotonic glucose (152 mM), EDNaClincreased by 3.6 mM, ( P < 0.01) without changes in renal hemodynamics, urine flow, sodium excretion rate, or PRC. Infusion of 300 μmol NaCl in a smaller volume caused EDNaCl to increase by 6.4 mM without significant changes in PRC. Urine flow and sodium excretion increased significantly. There was a significant inverse relationship between superficial nephron EDNaCl and PRC. We conclude that EDNa decreases during osmotic diuresis, suggesting that the increase in PRC was mediated by the macula densa. The results suggest that the natriuresis during osmotic diuresis is a result of impaired sodium reabsorption in distal tubules and collecting ducts.


1979 ◽  
Vol 84 (2) ◽  
pp. 163-171 ◽  
Author(s):  
A.-C. Ericson ◽  
M. Sjöquist ◽  
H. R. Ulfendahl

1964 ◽  
Vol 68 (5) ◽  
pp. 652-660 ◽  
Author(s):  
Lerner B. Hinshaw ◽  
Thomas E. Emerson ◽  
Charles M. Brake
Keyword(s):  

1985 ◽  
Vol 38 (6) ◽  
pp. 582-591 ◽  
Author(s):  
Mitchell P. Fink ◽  
Ronald Nelson ◽  
Rudolph Roethel
Keyword(s):  

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