scholarly journals Mechanism of trypsin-induced endothelium-dependent relaxation in porcine coronary artery

2000 ◽  
Vol 82 ◽  
pp. 188
Author(s):  
Tetsuzo Nakayama ◽  
Katsuya Hirano ◽  
Junji Nishimura ◽  
Hideo Kanaide
Keyword(s):  
Coronary Artery ◽  
Porcine Coronary Artery ◽  
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.

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

Lipids ◽  
2017 ◽  
Vol 52 (3) ◽  
pp. 235-243 ◽  
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

PLATELETS, ENDOTHELIUM AND VASOSPASM

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.

Effects of Thiopental on Endothelium-Dependent Relaxation in Porcine Coronary Arteries

2009 ◽  
Vol 37 (4) ◽  
pp. 1011-1017 ◽  
Author(s):  
O Dagtekin ◽  
HJ Gerbershagen ◽  
E Özgür ◽  
J Gaertner ◽  
JH Fischer
Keyword(s):  
Nitric Oxide ◽  
Coronary Artery ◽  
Coronary Arteries ◽  
Relaxation Response ◽  
Nitric Oxide Production ◽  
Porcine Coronary Artery ◽  
Relevant Concentration ◽  
Oxide Production ◽  
Prostaglandin F ◽  
Endothelium Dependent Relaxation

This study investigated the effects of thiopental on endothelium-dependent relaxation (EDR), and especially the effects on nitric oxide-and prostacyclin-independent EDR. Fresh porcine coronary artery rings (4 mm long), were consecutively tested with and without 20 μg/ml thiopental in Krebs–Henseleit solution. Indomethacin (10 μmol/1) was used in all experiments to eliminate prostacyclin effects. Prostaglandin F2α (10 μmol/l) was used to induce contractions and bradykinin (10−10−10−5 M) was used to induce EDR. Experiments were also carried out using 300 μmol/1 N-nitro-l-arginine to block nitric oxide production and to assess the influence of thiopental on nitric oxide-and prostacyclin-independent EDR. Thiopental induced statistically significant increases in EDR at concentrations of 10−6−10−5 M bradykinin. Following nitric oxide production block, thiopental significantly reduced the relaxation response at concentrations of 10−8−10−5 M bradykinin. At a clinically relevant concentration of 20 μg/ml thiopental, a significant increase in EDR and a significant reduction in nitric oxide-and prostacyclin-independent relaxation was observed in porcine epicardial coronary arteries.

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