Dilation of Retinal Arterioles in Response to Lactate: Role of Nitric Oxide, Guanylyl Cyclase, and ATP-Sensitive Potassium Channels

2006 ◽  
Vol 47 (2) ◽  
pp. 693 ◽  
Author(s):  
Travis W. Hein ◽  
Wenjuan Xu ◽  
Lih Kuo
Keyword(s):  
Nitric Oxide ◽  
Potassium Channels ◽  
Guanylyl Cyclase ◽  
Retinal Arterioles

scholarly journals Role of the nitric oxide–soluble guanylyl cyclase pathway in obstructive airway diseases

2014 ◽  
Vol 29 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Lisa L. Dupont ◽  
Constantinos Glynos ◽  
Ken R. Bracke ◽  
Peter Brouckaert ◽  
Guy G. Brusselle
Keyword(s):  
Nitric Oxide ◽  
Guanylyl Cyclase ◽  
Soluble Guanylyl Cyclase ◽  
Airway Diseases ◽  
Obstructive Airway Diseases

In vivo location and mechanism of EDHF-mediated vasodilation in canine coronary microcirculation

1999 ◽  
Vol 277 (3) ◽  
pp. H1252-H1259 ◽  
Author(s):  
Yasuhiro Nishikawa ◽  
David W. Stepp ◽  
William M. Chilian
Keyword(s):  
Nitric Oxide ◽  
Potassium Channels ◽  
Potassium Channel ◽  
Direct Evidence ◽  
Coronary Microcirculation ◽  
Combined Administration ◽  
Cytochrome P 450 ◽  
Coronary Arterioles

Responses of epicardial coronary arterioles to ACh were measured using stroboscopic fluorescence microangiography in dogs ( n = 38). ACh (0.1 and 0.5 μg ⋅ kg−1 ⋅ min−1ic) dilated small (<100 μm, 11 ± 2 and 19 ± 2%, respectively) and large (>100 μm, 6 ± 3 and 13 ± 3%, respectively) arterioles at baseline. Combined administration of N ω-monomethyl-l-arginine (l-NMMA; 1.0 μmol/min ic) and indomethacin (10 mg/kg iv) eliminated ACh-induced dilation in large coronary arterioles but only partially attenuated that in small arterioles. Suffusion of a buffer containing 60 mM KCl (high KCl) completely abolished cromakalim-induced dilation in arterioles and in combination with l-NMMA plus indomethacin completely blocked ACh-induced dilation in small arterioles. This indicated that the vasodilation to ACh that persists in small arterioles after administration of l-NMMA and indomethacin is mediated via a hyperpolarizing factor. The ACh-induced vasodilation remaining after l-NMMA and indomethacin was completely blocked by the large-conductance potassium-channel antagonist iberiotoxin or by epicardial suffusion of miconazole or metyrapone, inhibitors of cytochrome P-450 enzymes. These observations are consistent with the view that endothelium-derived hyperpolarizing factor (EDHF) is a product of cytochrome P-450 enzymes and produces vasodilation by the opening of large-conductance potassium channels. We conclude that ACh-induced dilation in large coronary arterioles is mediated mainly by nitric oxide (NO), whereas, in small arterioles both NO and EDHF mediate dilation to ACh. These data provide the first direct evidence for an in vivo role of EDHF in small coronary arterioles.

Role of Nitric Oxide and Potassium Channels in the Cholinergic Relaxation of Rabbit Ear and Femoral Arteries: Effects of Cooling

1995 ◽  
Vol 32 (6) ◽  
pp. 387-397 ◽  
Author(s):  
Angel Luis García-Villalón ◽  
Nuria Fernández ◽  
Luis Monge ◽  
José Luis García ◽  
Bernardino Gómez ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Potassium Channels ◽  
Femoral Arteries ◽  
Rabbit Ear

Novel guanylyl cyclase inhibitor, ODQ reveals role of nitric oxide, but not of cyclic GMP in endothelin-1 secretion

FEBS Letters ◽  
1995 ◽  
Vol 376 (3) ◽  
pp. 262-266 ◽  
Author(s):  
Friedrich Brunner ◽  
Heike Stessel ◽  
Walter R. Kukovetz
Keyword(s):  
Nitric Oxide ◽  
Cyclic Gmp ◽  
Guanylyl Cyclase ◽  
Endothelin 1
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