Terminalia avicennioides causes redox-sensitive endothelium-dependent relaxation involving nitric oxide, prostacyclin, and endothelium-derived hyperpolarizing in porcine coronary artery and different conductance and resistance vessels from rats

2020 ◽  
pp. 1
Author(s):  
Mbaye Sene ◽  
Hyunho Lee ◽  
Ibrahima Diouf ◽  
Maimouna Toure ◽  
Cathrine Senecheau ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Coronary Artery ◽  
Porcine Coronary Artery ◽  
Resistance Vessels ◽  
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.

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.

Hyperkalemia alters EDHF-mediated hyperpolarization and relaxation in coronary arteries

1996 ◽  
Vol 271 (2) ◽  
pp. H760-H767 ◽  
Author(s):  
G. W. He ◽  
C. Q. Yang ◽  
W. F. Graier ◽  
J. A. Yang
Keyword(s):  
Nitric Oxide ◽  
Cardiac Surgery ◽  
Smooth Muscle ◽  
Membrane Potential ◽  
Organ Preservation ◽  
Maximal Response ◽  
K Channels ◽  
Porcine Coronary Artery ◽  
Preservation Solutions ◽  
Endothelium Dependent Relaxation

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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