O11 Endothelium-dependent relaxation by a hydroethanolic extract of Adansonia digitata leaves in porcine coronary artery rings and rat thoracic aorta, mesenteric, carotid artery rings: Role of NO and EDH

2017 ◽  
Vol 139 ◽  
pp. 113
Author(s):  
Mbaye Sene ◽  
Modou Oumy Kane ◽  
Hyunho Lee ◽  
Cyril Auger ◽  
Philippe Chabert ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Carotid Artery ◽  
Thoracic Aorta ◽  
Adansonia Digitata ◽  
Porcine Coronary Artery ◽  
Rat Thoracic Aorta ◽  
Hydroethanolic Extract ◽  
Endothelium Dependent Relaxation

Two mechanisms mediate relaxation by bradykinin of pig coronary artery: NO-dependent and -independent responses

1991 ◽  
Vol 261 (3) ◽  
pp. H830-H835 ◽  
Author(s):  
C. L. Cowan ◽  
R. A. Cohen
Keyword(s):  
Nitric Oxide ◽  
Methylene Blue ◽  
Coronary Artery ◽  
Thromboxane A2 ◽  
Porcine Coronary Artery ◽  
Cyclic Monophosphate ◽  
Pig Coronary Artery ◽  
Endothelium Dependent Relaxation

The role of nitric oxide and guanosine 3',5'-cyclic monophosphate (cGMP) accumulation in the endothelium-dependent relaxation of the porcine coronary artery to bradykinin was investigated by comparing relaxation and cGMP accumulation in the presence or absence of NG-monomethyl-L-arginine (L-NMMA) and methylene blue. Rings were treated with indomethacin to eliminate the effects of prostaglandins. Relaxation to bradykinin of rings contracted with the thromboxane A2 mimetic U-46619 was not affected by L-NMMA and was only minimally inhibited by methylene blue. Rings contracted with elevated potassium (25 mM) also relaxed completely to bradykinin. However, L-NMMA or methylene blue effectively inhibited relaxation to bradykinin in rings contracted with potassium. cGMP accumulation was stimulated by bradykinin and inhibited by L-NMMA or methylene blue in rings contracted with either U-46619 or potassium. These results suggest that in the absence of nitric oxide-induced cGMP accumulation, a nonprostanoid mechanism exists that is capable of completely relaxing U-46619-contracted coronary artery. This mechanism is either inhibited in or unable to relax potassium-contracted rings. These results also demonstrate that nitric oxide mediates the bradykinin-induced cGMP accumulation that is largely responsible for the relaxation during contraction with potassium.

Lysophosphatidylcholine Inhibits Endothelium-Dependent Hyperpolarization and N ω -Nitro- l -Arginine/IndomethacinResistant Endothelium-Dependent Relaxation in the Porcine Coronary Artery

Circulation ◽  
1995 ◽  
Vol 92 (12) ◽  
pp. 3520-3526 ◽  
Author(s):  
Hiroshi Eizawa ◽  
Yoshiki Yui ◽  
Reiko Inoue ◽  
Kunihiko Kosuga ◽  
Ryuichi Hattori ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Porcine Coronary Artery ◽  
Endothelium Dependent Relaxation

Enhanced role of K+ channels in relaxations of hypercholesterolemic rabbit carotid artery to NO

1995 ◽  
Vol 269 (3) ◽  
pp. H805-H811 ◽  
Author(s):  
S. Najibi ◽  
R. A. Cohen
Keyword(s):  
Carotid Artery ◽  
Sodium Nitroprusside ◽  
Channel Blocker ◽  
Isometric Tension ◽  
K Channel ◽  
K Channels ◽  
Rabbit Carotid Artery ◽  
Cyclic Monophosphate ◽  
Endothelium Dependent Relaxation

Endothelium-dependent relaxations to acetylcholine remain normal in the carotid artery of hypercholesterolemic rabbits, but unlike endothelium-dependent relaxations of normal rabbits, they are inhibited by charybdotoxin, a specific blocker of Ca(2+)-dependent K+ channels. Because nitric oxide (NO) is the mediator of endothelium-dependent relaxation and can activate Ca(2+)-dependent K+ channels directly or via guanosine 3',5'-cyclic monophosphate, the present study investigated the role of Ca(2+)-dependent K+ channels in relaxations caused by NO, sodium nitroprusside, and 8-bromoguanosine 3',5'-cyclic monophosphate (8-Brc-GMP) in hypercholesterolemic rabbit carotid artery. Isometric tension was measured in rabbit carotid artery denuded of endothelium from normal and hypercholesterolemic rabbits which were fed 0.5% cholesterol for 12 wk. Under control conditions, relaxations to all agents were similar in normal and hypercholesterolemic rabbit arteries. Charybdotoxin had no significant effect on relaxations of normal arteries to NO, sodium nitroprusside, or 8-BrcGMP, but the Ca(2+)-dependent K+ channel blocker significantly inhibited the relaxations caused by each of these agents in the arteries from hypercholesterolemic rabbits. By contrast, relaxations to the calcium channel blocker nifedipine were potentiated to a similar extent by charybdotoxin in both groups. In addition, arteries from hypercholesterolemic rabbits relaxed less than normal to sodium nitroprusside when contracted with depolarizing potassium solution. These results indicate that although nitrovasodilator relaxations are normal in the hypercholesterolemic rabbit carotid artery, they are mediated differently, and to a greater extent, by Ca(2+)-dependent K+ channels. These data also suggest that K+ channel-independent mechanism(s) are impaired in hypercholesterolemia.

Puerarin protects against high glucose-induced acute vascular dysfunction: Role of heme oxygenase-1 in rat thoracic aorta

2009 ◽  
Vol 50 (3-4) ◽  
pp. 110-115 ◽  
Author(s):  
Xiang-hong Meng ◽  
Chao Ni ◽  
Li Zhu ◽  
Yue-liang Shen ◽  
Lin-lin Wang ◽  
...  
Keyword(s):  
Thoracic Aorta ◽  
Heme Oxygenase ◽  
High Glucose ◽  
Vascular Dysfunction ◽  
Heme Oxygenase 1 ◽  
Rat Thoracic Aorta

Procyanidin-rich fractions from Parkia biglobosa (Mimosaceae) leaves cause redox-sensitive endothelium-dependent relaxation involving NO and EDHF in porcine coronary artery

2010 ◽  
Vol 132 (1) ◽  
pp. 246-250 ◽  
Author(s):  
Jean-Marie Tokoudagba ◽  
Cyril Auger ◽  
Lise Bréant ◽  
Saliou N’Gom ◽  
Philippe Chabert ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Parkia Biglobosa ◽  
Porcine Coronary Artery ◽  
Endothelium Dependent Relaxation
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