scholarly journals Nitroarginine-Sensitive and -Insensitive Components of the Endothelium-Dependent Relaxation in the Guinea-Pig Carotid Artery.

1992 ◽  
Vol 42 (2) ◽  
pp. 335-347 ◽  
Author(s):  
Hikaru SUZUKI ◽  
Guifa CHEN ◽  
Yoshimichi YAMAMOTO ◽  
Kyoko MIWA
Keyword(s):  
Carotid Artery ◽  
Guinea Pig ◽  
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.

scholarly journals Role of endothelial cell hyperpolarization in EDHF-mediated responses in the guinea-pig carotid artery

2000 ◽  
Vol 129 (6) ◽  
pp. 1103-1112 ◽  
Author(s):  
J -F Quignard ◽  
M Félétou ◽  
G Edwards ◽  
J Duhault ◽  
A H Weston ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Carotid Artery ◽  
Guinea Pig

Differential effects of prostacyclin and iloprost in the isolated carotid artery of the guinea-pig

2001 ◽  
Vol 426 (1-2) ◽  
pp. 89-94 ◽  
Author(s):  
Catherine Corriu ◽  
Michel Félétou ◽  
Gillian Edwards ◽  
Arthur H. Weston ◽  
Paul M. Vanhoutte
Keyword(s):  
Carotid Artery ◽  
Guinea Pig ◽  
Differential Effects

scholarly journals Effect of Chronic Treatment with Perindopril on Endothelium-dependent Relaxation of Aorta and Carotid Artery in SHRSP.

2000 ◽  
Vol 36 (1) ◽  
pp. 33-46 ◽  
Author(s):  
Keiichi SHIMAMURA ◽  
Fumiko SEKIGUCHI ◽  
Kyoko MATSUDA ◽  
Mirei OZAKI ◽  
Kiyomi NOGUCHI ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Chronic Treatment ◽  
Endothelium Dependent Relaxation

scholarly journals Role of SKCa and IKCa in endothelium-dependent hyperpolarizations of the guinea-pig isolated carotid artery

2005 ◽  
Vol 144 (4) ◽  
pp. 477-485 ◽  
Author(s):  
Pascale Gluais ◽  
Gillian Edwards ◽  
Arthur H Weston ◽  
John R Falck ◽  
Paul M Vanhoutte ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Guinea Pig

scholarly journals Inhibition of the Endothelium-Dependent Relaxation by 18.BETA.-Glycyrrhetinic Acid in the Guinea-Pig Aorta.

1999 ◽  
Vol 49 (3) ◽  
pp. 267-274 ◽  
Author(s):  
Hiroyasu FUKUTA ◽  
Makoto KOSHITA ◽  
Yoshimichi YAMAMOTO ◽  
Hikaru SUZUKI
Keyword(s):  
Guinea Pig ◽  
Glycyrrhetinic Acid ◽  
Endothelium Dependent Relaxation

scholarly journals Chronic in vivo or acute in vitro resveratrol attenuates endothelium-dependent cyclooxygenase-mediated contractile signaling in hypertensive rat carotid artery

2016 ◽  
Vol 120 (10) ◽  
pp. 1141-1150 ◽  
Author(s):  
Steven G. Denniss ◽  
Rebecca J. Ford ◽  
Christopher S. Smith ◽  
Andrew J. Jeffery ◽  
James W. E. Rush
Keyword(s):  
Carotid Artery ◽  
Day Treatment ◽  
Spontaneously Hypertensive ◽  
Compound C ◽  
Tp Receptor ◽  
Wistar Kyoto ◽  
Amp Activated Protein Kinase ◽  
Endothelium Dependent Relaxation

Exaggerated cyclooxygenase (COX) and thromboxane-prostanoid (TP) receptor-mediated endothelium-dependent contraction can contribute to endothelial dysfunction. This study examined the effect of resveratrol (RSV) on endothelium-dependent contraction and cell signaling in the common carotid artery (CCA) from spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY). Acetylcholine (Ach)-stimulated endothelium-dependent nitric oxide synthase (NOS)-mediated relaxation in precontracted SHR CCA was impaired (maximum 73 ± 6% vs. 87 ± 5% in WKY) ( P < 0.05) by competitive COX-mediated contraction. Chronic (28-day) treatment in vivo (drinking water) with a ∼0.075 mg·kg−1·day−1 RSV dose affected neither endothelium-dependent relaxation nor endothelium-dependent contraction and associated prostaglandin (PG) production evaluated in non-precontracted NOS-blocked CCA. In contrast, a chronic ∼7.5 mg·kg−1·day−1 RSV dose improved endothelium-dependent relaxation (94 ± 6%) and attenuated endothelium-dependent contraction (58 ± 4% vs. 73 ± 5% in No-RSV) and PG production (183 ± 43 vs. 519 ± 93 pg/ml) in SHR CCA, while U46619-stimulated TP receptor-mediated contraction was unaffected. In separate acute in vitro experiments, 20-μM RSV preincubation attenuated endothelium-dependent contraction (6 ± 4% vs. 62 ± 2% in No Drug) and PG production (121 ± 15 vs. 491 ± 93 pg/ml) and attenuated U46619-stimulated contraction (134 ± 5% vs. 171 ± 4%) in non-precontracted NOS-blocked SHR CCA. Compound C, a known AMP-activated protein kinase (AMPK) inhibitor, did not prevent the RSV attenuating effect on Ach- and U46619 -stimulated contraction but did prevent the RSV attenuating effect on PG production (414 ± 58 pg/ml). These data demonstrate that RSV can attenuate endothelium-dependent contraction both by suppressing arterial wall PG production, which may be partially mediated by AMPK, and by TP receptor hyporesponsiveness, which does not appear to be mediated by AMPK.

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