Involvement of potassium channels in the protective effect of 17β-estradiol on hypercholesterolemic rabbit carotid artery

2000 ◽  
Vol 152 (1) ◽  
pp. 59-67 ◽  
Author(s):  
Khadija Ghanam ◽  
Leng Ea-Kim ◽  
James Javellaud ◽  
Nicole Oudart
Keyword(s):  
Carotid Artery ◽  
Potassium Channels ◽  
Protective Effect ◽  
Rabbit Carotid Artery ◽  
17Β Estradiol

Enhanced role of potassium channels in relaxations to acetylcholine in hypercholesterolemic rabbit carotid artery

1994 ◽  
Vol 266 (5) ◽  
pp. H2061-H2067 ◽  
Author(s):  
S. Najibi ◽  
C. L. Cowan ◽  
J. J. Palacino ◽  
R. A. Cohen
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Carotid Artery ◽  
Potassium Channels ◽  
Abdominal Aorta ◽  
Combined Treatment ◽  
Rabbit Carotid Artery ◽  
Calcium Dependent ◽  
Endothelium Dependent Relaxation

The effect of hypercholesterolemia for 10 wk on endothelium-dependent relaxations to acetylcholine was studied in isolated rings of rabbit carotid artery and abdominal aorta contracted with phenylephrine or elevated potassium. In these arteries obtained from hypercholesterolemic rabbits, endothelium-dependent relaxations to acetylcholine were not significantly different from those of normal rabbits. In normal and hypercholesterolemic arteries, partial relaxation persisted in the presence of NG-nitro-L-arginine methyl ester (L-NAME), which blocked acetylcholine-induced increases in arterial guanosine 3',5'-cyclic monophosphate (cGMP). Combined treatment with L-NAME and the calcium-dependent potassium-channel inhibitor, charybdotoxin, blocked relaxations in both groups, suggesting that L-NAME-resistant relaxations are mediated by an endothelium-derived hyperpolarizing factor. Charybdotoxin alone or depolarizing potassium had no significant effect on normal carotid artery or normal and hypercholesterolemic abdominal aorta but significantly inhibited relaxations of the carotid artery from cholesterol-fed rabbits. The enhanced role of calcium-dependent potassium channels and the hyperpolarizing factor in relaxation of the hypercholesterolemic carotid artery suggested by these results was likely related to the fact that acetylcholine failed to stimulate cGMP only in that artery. These data suggest that endothelium-dependent relaxation in these rabbit arteries is mediated by nitric oxide-cGMP-dependent and -independent mechanisms. In hypercholesterolemia, the contribution of nitric oxide-cGMP in the carotid artery is reduced, but a hyperpolarizing factor and calcium-dependent potassium channels maintain normal acetylcholine-induced relaxation.

Involvement of prostacyclin and potassium channels in the diabetes-induced hyporeactivity of the rabbit carotid artery to B-type natriuretic peptide

2013 ◽  
Vol 701 (1-3) ◽  
pp. 159-167 ◽  
Author(s):  
José M. Centeno ◽  
Vannina G. Marrachelli ◽  
Luis Miranda ◽  
María Castelló-Ruiz ◽  
María C. Burguete ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Potassium Channels ◽  
Natriuretic Peptide ◽  
Rabbit Carotid Artery

Potassium channels contribute to the increased sensitivity of the rabbit carotid artery to hydrogen sulfide in diabetes

2019 ◽  
Vol 853 ◽  
pp. 33-40 ◽  
Author(s):  
José M. Centeno ◽  
Mikahela A. López-Morales ◽  
Alicia Aliena-Valero ◽  
Teresa Jover-Mengual ◽  
María C. Burguete ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Carotid Artery ◽  
Potassium Channels ◽  
Rabbit Carotid Artery ◽  
Increased Sensitivity

Effect of atherosclerosis on responses of the perfused rabbit carotid artery to human platelets.

1992 ◽  
Vol 12 (10) ◽  
pp. 1206-1213 ◽  
Author(s):  
S Kaul ◽  
R C Padgett ◽  
B J Waack ◽  
R M Brooks ◽  
D D Heistad
Keyword(s):  
Carotid Artery ◽  
Human Platelets ◽  
Rabbit Carotid Artery

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 Pharmacogenomics of estrogens on changes in carotid artery intima-medial thickness and coronary arterial calcification: Kronos Early Estrogen Prevention Study

2016 ◽  
Vol 48 (1) ◽  
pp. 33-41 ◽  
Author(s):  
Virginia M. Miller ◽  
Gregory D. Jenkins ◽  
Joanna M. Biernacka ◽  
John A. Heit ◽  
Gordon S. Huggins ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Carotid Artery ◽  
Hormone Treatment ◽  
Arterial Calcification ◽  
Nucleotide Polymorphisms ◽  
Prevention Study ◽  
Conjugated Equine Estrogens ◽  
17Β Estradiol ◽  
Innate Immunity Pathway ◽  
Intima Medial Thickness

Prior to the initiation of menopausal hormone treatment (MHT), genetic variations in the innate immunity pathway were found to be associated with carotid artery intima-medial thickness (CIMT) and coronary arterial calcification (CAC) in women ( n = 606) enrolled in the Kronos Early Estrogen Prevention Study (KEEPS). Whether MHT might affect these associations is unknown. The association of treatment outcomes with variation in the same 764 candidate genes was evaluated in the same KEEPS participants 4 yr after randomization to either oral conjugated equine estrogens (0.45 mg/day), transdermal 17β-estradiol (50 μg/day), each with progesterone (200 mg/day) for 12 days each month, or placebo pills and patch. Twenty SNPs within the innate immunity pathway most related with CIMT after 4 yr were not among those associated with CIMT prior to MHT. In 403 women who completed the study in their assigned treatment group, single nucleotide polymorphisms (SNPs) within the innate immunity pathway were found to alter the treatment effect on 4 yr change in CIMT (i.e., significant interaction between treatment and genetic variation in the innate immunity pathway; P < 0.001). No SNPs by treatment effects were observed with changes of CAC >5 Agatston units after 4 yr. Results of this study suggest that hormonal status may interact with genetic variants to influence cardiovascular phenotypes, specifically, the pharmacogenomic effects within the innate immunity pathway for CIMT.

The Antiaggregating and Antithrombotic Activity of Clopidogrel Is Potentiated by Aspirin in Several Experimental Models in the Rabbit

1998 ◽  
Vol 80 (09) ◽  
pp. 512-518 ◽  
Author(s):  
Frédérique Dol ◽  
André Bernat ◽  
Robert Falotico ◽  
Alain Lalé ◽  
Pierre Savi ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Carotid Artery ◽  
Ex Vivo ◽  
Thrombus Formation ◽  
Experimental Models ◽  
Arteriovenous Shunt ◽  
Thrombotic Occlusion ◽  
Antithrombotic Activity ◽  
Rabbit Carotid Artery ◽  
Antithrombotic Efficacy

SummaryIt is unknown whether the addition of aspirin might increase both the efficacy and the potency of clopidogrel, a potent and selective ADP blocker. For that purpose, the efficacy of clopidogrel (1–20 mg/kg, p.o.) administered orally to rabbits alone or in combination with aspirin (0.1–10 mg/kg, p.o.) was determined in several experimental models. A potent synergistic effect of the clopidogrel/aspirin association was demonstrated with regard to collagen-induced platelet aggregation measured ex vivo. Similarly, aspirin potentiated the antithrombotic activity of clopidogrel measured with regard to experimental thrombosis induced by a silk thread or on stents placed in an arteriovenous shunt, thrombus formation following electrical stimulation of the rabbit carotid artery and with regard to 111In-labeled platelet deposition on a stent implanted in an arteriovenous shunt or on the subendothelium following air drying injury of the rabbit carotid artery. A similar potentiating effect of aspirin was obtained with regard to myointimal proliferation (restenosis) in the femoral arteries of atherosclerotic rabbits which occurred as a consequence of stent placement. The clopidogrel/aspirin combination showed only additive-type effects on bleeding time prolongation induced by ear transection in the rabbit, therefore showing that combined inhibition of cyclooxygenase and ADP‘s effects provide a marked enhanced antithrombotic efficacy. Such a combination may provide substantial protection against platelet aggregation leading to thrombotic occlusion at sites of endothelial injuries and coronary artery stenosis in humans.

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