Both Nitric Oxide and Endothelin-1 Influence Cerebral Blood Flow Velocity at Rest and after Hyper- and Hypocapnic Stimuli in Hypertensive and Healthy Adolescents

2006 ◽  
Vol 29 (3) ◽  
pp. 152-158 ◽  
Author(s):  
Éva Katona ◽  
Georgios Settakis ◽  
Zsuzsa Varga ◽  
Mária Juhász ◽  
György Paragh ◽  
...  
1995 ◽  
Vol 15 (3) ◽  
pp. 519-524 ◽  
Author(s):  
Patrick Hylland ◽  
Göran E. Nilsson

Nitric oxide (NO)–dependent regulation of brain blood flow has not been proven to exist in fish or other ectothermic vertebrates. Using epi-illumination microscopy on the brain surface (optic lobes) of crucian carp ( Carassius carassius), we show that superfusing the brain with acetylcholine (ACh) induces an increase in cerebral blood flow velocity that can be completely blocked by the NO synthase inhibitors NG-nitro-l-arginine methylester (L-NAME) and NG-nitro-l-arginine. Also, sodium nitroprusside, which decomposes to liberate NO, causes an increase in cerebral blood flow velocity. By contrast, L-NAME does not block the increase in blood flow velocity caused by anoxia. The results suggest that NO is an endogenous vasodilator in crucian carp brain that mediates the effects of ACh. Because teleost fish deviated from other vertebrates 400 million years ago, these results suggest that NO-dependent brain blood flow regulation was an early event in vertebrate evolution.


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