Kaempferol enhances endothelium-dependent relaxation in the porcine coronary artery through activation of large-conductance Ca2+-activated K+channels

Hyperkalemic solutions are widely used to preserve organs for transplantation and for cardiac surgery. The present study was designed to test the hypothesis that hyperkalemia may alter endothelial function through a non-nitric oxide (NO) pathway, since preliminary studies have shown that the NO pathway may not be affected. Porcine coronary artery rings were studied in organ chambers. After incubation with 20 or 50 mM K+ for 1 h, the indomethacin- and NG-nitro-L-arginine+ (L-NNA)-resistant relaxation induced by A23187 or bradykinin, which could be further inhibited by tetraethylammonium but not glibenclamide, was significantly reduced. Incubation with hyperkalemia also significantly increased the concentration eliciting 50% of the maximal response to A23187 and bradykinin. A23187-induced hyperpolarization of the membrane potential was significantly reduced by hyperkalemic incubation. However, 1-h incubation with hyperkalemia does not affect the endothelial Ca2+ concentration. We conclude that exposure to hyperkalemia reduces the indomethacin- and L-NNA-resistant endothelium-dependent relaxation and endothelium-dependent hyperpolarization. This reduction in the relaxation and hyperpolarization is related to the endothelium-derived hyperpolarizing factor by affecting its effect on the smooth muscle cell, probably through partially depolarizing the membrane, and the Ca2(+)- activated K+ channels rather than by affecting its biosynthesis and/or release in the endothelial cell. Our study may suggest a new mechanism for coronary dysfunction after exposure to hyperkalemic cardioplegia and organ preservation solutions.

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Involvement of K+ Channels in Adenosine A2A and A2B Receptor-Mediated Hyperpolarization of Porcine Coronary Artery Endothelial Cells

Journal of Cardiovascular Pharmacology ◽

10.1097/00005344-200207000-00006 ◽

2002 ◽

Vol 40 (1) ◽

pp. 43-49 ◽

Cited By ~ 15

Author(s):

Hammed A. Olanrewaju ◽

B. S. Gafurov ◽

E. M. Lieberman

Keyword(s):

Endothelial Cells ◽

Coronary Artery ◽

K Channels ◽

Porcine Coronary Artery ◽

A2b Receptor ◽

Adenosine A2a

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

Journal of Ethnopharmacology ◽

10.1016/j.jep.2010.08.031 ◽

2010 ◽

Vol 132 (1) ◽

pp. 246-250 ◽

Cited By ~ 16

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

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1991.261.3.h830 ◽

1991 ◽

Vol 261 (3) ◽

pp. H830-H835 ◽

Cited By ~ 13

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.

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Lipid Emulsions Containing Medium Chain Triacylglycerols Blunt Bradykinin-Induced Endothelium-Dependent Relaxation in Porcine Coronary Artery Rings

Lipids ◽

10.1007/s11745-016-4225-y ◽

2017 ◽

Vol 52 (3) ◽

pp. 235-243 ◽

Cited By ~ 2

Author(s):

Said Amissi ◽

Julie Boisramé-Helms ◽

Mélanie Burban ◽

Sherzad K. Rashid ◽

Antonio J. León-González ◽

...

Keyword(s):

Coronary Artery ◽

Lipid Emulsions ◽

Porcine Coronary Artery ◽

Medium Chain ◽

Endothelium Dependent Relaxation

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PLATELETS, ENDOTHELIUM AND VASOSPASM

10.1055/s-0038-1643722 ◽

1987 ◽

Author(s):

Paul M Vanhoutte

Keyword(s):

Coronary Artery ◽

Blood Vessels ◽

Coronary Arteries ◽

Adenine Nucleotides ◽

Platelet Activating Factor ◽

Protective Role ◽

Human Platelets ◽

Porcine Coronary Artery ◽

Paf Antagonists ◽

Endothelium Dependent Relaxation

The endothelium can secrete both relaxing and contracting substances. One of the most powerful stimuli to the release of the former are thrombin and aggregating platelets. This contributes to the protective role of the endothelium against inappropriate intraluminal platelet aggregation and coagulation in blood vessels with an intact intima. Thrombin-induced, endothelium-dependent relaxations have been obtained in isolated arteries of different species, including humans. Endothelium-dependent relaxations can be evoked by autologous platelets in isolated blood vessels of the dog, pig and rat; they can be obtained in canine coronary arteries with human platelets. The major platelet-products involved in these endothelium-dependent relaxations are 5-hydroxytryptamine (serotonin) and the adenine nucleotides. Although platelet-activating factor (PAF) can evoke endothelium-dependent relaxation it only does so at concentrations much higher than those occurring under physiological conditions; since the relaxations are not prevented by PAF-antagonists, they are non-specific in nature.The receptor mediating the endothelium-dependent relaxations to serotonin released from the aggregating platelets can be subtyped as a S1~(5HT1) serotonergic receptor;those mediating the response to the adenine nucleotides as P2y-purinergic receptors. In the absence of the endothelium aggregating platelets cause contractions of vascular smooth muscle; these are mediated by a mixture of S1-like and S2~serotoner-gic receptors in coronary arteriesof the dog, and by S2-serotonergic receptors in those of the pig. Thus, in the porcine coronary artery, the S2-serotonergic antagonist ketanserin markedly enhances the platelet-induced endothelium-dependent relaxation. After previous (four weeks) injury, the regenerated endothelium of the porcine coronary artery loses the ability to respond to serotonin,and is unable to prevent the constrictionsevoked by aggregating platelets. The endothelium-dependent relaxations of porcine coronary arteries evoked by aggregating platelets are potentiated by chronic treatmentof the donor animals with cod liver oil. These studies emphasize the protective roleof the endothelial cells against the vasoconstriction (vasospasm) induced by aggregating platelets. This role is depressed after previous injury, and can be facilitatedby dietary adj ustments.

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