Role of nitric oxide in local blood flow control in the anaesthetized dog

1992 ◽  
Vol 420 (2) ◽  
pp. 194-199 ◽  
Author(s):  
Michael Sonntag ◽  
Andreas Deussen ◽  
J�rgen Schrader
2011 ◽  
Vol 49 (6) ◽  
pp. 627-629 ◽  
Author(s):  
Annemiek J. M. Cornelissen

2008 ◽  
Vol 33 (1) ◽  
pp. 151-160 ◽  
Author(s):  
Michael E. Tschakovsky ◽  
Michael J. Joyner

Despite being the subject of investigation for well over 100 years, the nature of exercising muscle blood flow control remains, in many respects, poorly understood. In this review we focus on the potential role of nitric oxide in vasodilation of muscle resistance vessels during a bout of exercise. Its contribution is explored in the context of whether it contributes to steady-state exercise hyperemia, the dynamic adjustment of muscle blood flow to exercise, or the modulation of sympathetic vasoconstriction in exercising muscle. It appears that the obligatory role of nitric oxide in all three of these categories is modest at best. The elucidation of the integrated nature of exercise hyperemia control in terms of synergy and redundancy of mechanism interaction remains in its infancy, and much more remains to be learned about the role of nitric oxide in this type of integrated control.


1978 ◽  
Vol 43 (5) ◽  
pp. 769-776 ◽  
Author(s):  
A H Goodman ◽  
R Einstein ◽  
H J Granger

2015 ◽  
Vol 98 (5) ◽  
pp. 3046-3058 ◽  
Author(s):  
T.G. Madsen ◽  
S.R.L. Cieslar ◽  
D.R. Trout ◽  
M.O. Nielsen ◽  
J.P. Cant

Hypertension ◽  
1995 ◽  
Vol 25 (3) ◽  
pp. 408-414 ◽  
Author(s):  
Francisco J. Fenoy ◽  
Paloma Ferrer ◽  
Luis Carbonell ◽  
Miguel García-Salom

2012 ◽  
Vol 13 (Suppl 1) ◽  
pp. A28
Author(s):  
Doreen Schmidl ◽  
Agnes Boltz ◽  
Semira Kaya ◽  
René Werkmeister ◽  
Reinhard Told ◽  
...  

2005 ◽  
Vol 289 (6) ◽  
pp. F1324-F1332 ◽  
Author(s):  
Manish M. Tiwari ◽  
Robert W. Brock ◽  
Judit K. Megyesi ◽  
Gur P. Kaushal ◽  
Philip R. Mayeux

Acute renal failure (ARF) is a frequent and serious complication of endotoxemia caused by lipopolysaccharide (LPS) and contributes significantly to mortality. The present studies were undertaken to examine the roles of nitric oxide (NO) and caspase activation on renal peritubular blood flow and apoptosis in a murine model of LPS-induced ARF. Male C57BL/6 mice treated with LPS ( Escherichia coli) at a dose of 10 mg/kg developed ARF at 18 h. Renal failure was associated with a significant decrease in peritubular capillary perfusion. Vessels with no flow increased from 7 ± 3% in the saline group to 30 ± 4% in the LPS group ( P < 0.01). Both the inducible NO synthase inhibitor l- N6-1-iminoethyl-lysine (l-NIL) and the nonselective caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp fluoromethylketone (Z-VAD) prevented renal failure and reversed perfusion deficits. Renal failure was also associated with an increase in renal caspase-3 activity and an increase in renal apoptosis. Both l-NIL and Z-VAD prevented these changes. LPS caused an increase in NO production that was blocked by l-NIL but not by Z-VAD. Taken together, these data suggest NO-mediated activation of renal caspases and the resulting disruption in peritubular blood flow are an important mechanism of LPS-induced ARF.


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