scholarly journals Inhibitory effect of cold storage on the endothelium dependent relaxation elicited by A23187 in hog coronary artery

1987 ◽  
Vol 43 ◽  
pp. 289
Author(s):  
Yukisato Ishida ◽  
Michio Hashimoto ◽  
Richard J. Paul
Keyword(s):  
Coronary Artery ◽  
Cold Storage ◽  
Inhibitory Effect ◽  
Endothelium Dependent Relaxation

BKCa channels compensate for loss of NOS-dependent coronary artery relaxation in cardiomyopathy

2000 ◽  
Vol 279 (6) ◽  
pp. H2598-H2603 ◽  
Author(s):  
Shawn G. Clark ◽  
Leslie C. Fuchs
Keyword(s):  
Nitric Oxide ◽  
Coronary Artery ◽  
Coronary Arteries ◽  
Late Stage ◽  
Inhibitory Effect ◽  
Bkca Channels ◽  
Small Arteries ◽  
Cardiomyopathic Hamsters ◽  
Oxide Synthase ◽  
Endothelium Dependent Relaxation

Previously, we showed that development of myocardial necrotic lesions is associated with impaired endothelium-dependent coronary artery relaxation in young cardiomyopathic hamsters. Since active necrosis declines with aging, this study was designed to determine whether coronary artery endothelium-dependent relaxation to ACh is restored and to identify the mechanisms mediating this effect. Intraluminal diameter was recorded in coronary arteries (150–250 μm) from control (C, 297 ± 5 days old) and cardiomyopathic (M, 296 ± 4 days old) hamsters. Relaxation to ACh (10−9–3 × 10−5M) was similar in vessels from C and M hamsters. However, mechanisms mediating relaxation to ACh were altered. Inhibition of nitric oxide synthase (NOS) activity with N-nitro-l-arginine (1 mM) had a greater inhibitory effect in vessels from C hamsters, indicating a reduction in NOS-dependent relaxation in vessels from M hamsters. Conversely, inhibition of large Ca2+-dependent K+ (BKCa) channels with charybdotoxin (CTX, 0.1 μM) had a greater inhibitory effect in vessels from M hamsters. In the presence of both N-nitro-l-arginine and CTX, relaxation to ACh was abolished in both groups. CTX (0.1 μM) produced a 50 ± 4 and 30 ± 3% contraction of vessels from M and C hamsters, respectively, indicating an enhanced role for BKCa channels in regulation of coronary artery tone in M hamsters. Finally, vasodilatory cyclooxygenase products contributed to ACh-induced relaxation in vessels from M, but not C, hamsters. In conclusion, NOS-dependent relaxation of coronary small arteries is reduced in the late stage of cardiomyopathy. An increase in relaxation mediated by BKCa channels and vasodilatory cyclooxygenase products compensates for this effect.

Characterization of Thromboxane A2/Prostaglandin H2 Receptors in Porcine Coronary Artery -The Inhibitory Effect of a Novel Dibenzoxepin Derivative, KW-3635

1992 ◽  
Vol 67 (05) ◽  
pp. 582-584 ◽  
Author(s):  
Ichiro Miki ◽  
Akio Ishii
Keyword(s):  
Coronary Artery ◽  
Binding Sites ◽  
Thromboxane A2 ◽  
Inhibitory Effect ◽  
Scatchard Analysis ◽  
Single Class ◽  
Porcine Coronary Artery ◽  
Equilibrium Binding ◽  
H2 Receptors

SummaryWe characterized the thromboxane A2/prostaglandin H2 receptors in porcine coronary artery. The binding of [3H]SQ 29,548, a thromboxane A2 antagonist, to coronary arterial membranes was saturable and displaceable. Scatchard analysis of equilibrium binding showed a single class of high affinity binding sites with a dissociation constant of 18.5 ±1.0 nM and the maximum binding of 80.7 ± 5.2 fmol/mg protein. [3H]SQ 29,548 binding was concentration-dependently inhibited by thromboxane A2 antagonists such as SQ 29,548, BM13505 and BM13177 or the thromboxane A2 agonists such as U46619 and U44069. KW-3635, a novel dibenzoxepin derivative, concentration-dependently inhibited the [3H]SQ 29,548 binding to thromboxane A2/prosta-glandin H2 receptors in coronary artery with an inhibition constant of 6.0 ± 0.69 nM (mean ± S.E.M.).

Endothelium derived relaxing factor release from canine coronary artery by leukocytes

1995 ◽  
Vol 73 (3) ◽  
pp. 404-408 ◽  
Author(s):  
Joseph F. Kleha ◽  
Pierre Devesly ◽  
Anthony Johns
Keyword(s):  
Endothelial Cell ◽  
Coronary Artery ◽  
Human Monocyte ◽  
Relaxing Factor ◽  
Canine Coronary Artery ◽  
Endothelium Derived Relaxing Factor ◽  
Ly 83583 ◽  
Muscle Calcium ◽  
Endothelium Dependent Relaxation ◽  
Factor Release

Lectins, known to recognize endothelial cell adhesion molecules, have been shown to release endothelium-derived relaxing factor (EDRF) from blood vessels. We investigated the effects of different leukocyte-type cells to determine if these cells, by interacting with the endothelium, could release EDRF from the circumflex branch of the canine coronary artery. The following cells were investigated: human promyelocytic leukemia (HL-60), human monocyte (THP-1), and human Burkitt lymphoma (DAUDI). All of these cells produced a significant endothelium-dependent relaxation of the dog coronary artery in the presence of ibuprofen. The endothelium-dependent relaxations were reversed by hemoglobin (10 μM), methylene blue (3 μM), 6-anilino-5,8-quinolinedione (LY 83583, 30 μM), and NG-nitro-L-arginine methyl ester (L-NAME, 1 mM). HL-60 cells grown in the presence of 1 mM L-NAME retained their ability to cause endothelium-dependent relaxation of the canine coronary artery, suggesting that the source of the NO was the endothelium and not the HL-60 cells. The cell-induced vascular relaxation could be obtained in the absence of extracellular calcium. It is suggested that HL-60, THP-1, and DAUDI cells interact with a specific receptor on the endothelial cell and as a result of this interaction the endothelial cells are stimulated to release EDRF.Key words: endothelium-derived relaxing factor, nitric oxide, endothelium, HL-60, DAUDI, THP-1, smooth muscle, calcium, contraction, canine coronary artery.

Increases in pulse pressure impair acetylcholine-induced vascular relaxation

1995 ◽  
Vol 268 (1) ◽  
pp. H359-H363 ◽  
Author(s):  
S. M. Ryan ◽  
B. J. Waack ◽  
B. L. Weno ◽  
D. D. Heistad
Keyword(s):  
Pulse Pressure ◽  
Carotid Arteries ◽  
Inhibitory Effect ◽  
Isometric Tension ◽  
High Pulse Pressure ◽  
Donor Artery ◽  
Mean Pressure ◽  
High Pulse ◽  
Endothelium Derived Relaxing Factor ◽  
Endothelium Dependent Relaxation

Effects of pulse pressure on acetylcholine-induced endothelium-dependent relaxation were investigated using a cascade bioassay model. Intact carotid arteries from rabbits were perfused at constant flow, and activity of endothelium-derived relaxing factor (EDRF) was assayed by measuring changes in isometric tension in a detector ring without endothelium. When pulse pressure of the donor artery was raised from approximately 2 to 10 mmHg, relaxation to acetylcholine (10(-7) M) was reduced from 31 +/- 3 (means +/- SE) to 20 +/- 2% (expressed as percent relaxation of phenylephrine-induced tone). Responses of the detector ring to nitroprusside were unchanged. Superoxide dismutase (SOD) and indomethacin each prevented impairment of relaxation to acetylcholine at high pulse pressure. When the donor artery was perfused at a higher mean pressure, elevation of pulse pressure also impaired relaxation to acetylcholine, and this impairment was prevented by SOD. These findings suggest that elevation of pulse pressure inhibits acetylcholine-induced, endothelium-dependent relaxation, and this inhibitory effect is mediated by generation of oxygen radicals.

U46619, a thromboxane A2 agonist, inhibits KCa channel activity from pig coronary artery

1992 ◽  
Vol 262 (3) ◽  
pp. C708-C713 ◽  
Author(s):  
F. S. Scornik ◽  
L. Toro
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Lipid Bilayers ◽  
Thromboxane A2 ◽  
Inhibitory Effect ◽  
Channel Activity ◽  
Open Probability ◽  
Control Value ◽  
Kca Channels ◽  
Internal Side

Thromboxane A2 (TxA2) is a potent vasoconstrictor derived from the metabolism of arachidonic acid. Because potassium channels are involved in the contraction of vascular smooth muscle, their blockade could contribute to the TxA2-induced contraction. To test this possibility, we studied the effect of the TxA2 stable analogue U46619 on calcium-activated potassium (KCa) channels from coronary artery reconstituted into lipid bilayers. Addition of U46619 (50-150 nM) to the external but not to the internal side of the channel decreased the channel open probability (Po) between 15 and 80% of the control value. The inhibitory effect of U46619 affected both the open and closed states of the channel and could be reversed by internal calcium. Thromboxane B2, the inactive hydrolysis derivative of TxA2, did not affect channel activity. SQ 29548, a TxA2 receptor antagonist, was able to prevent the inhibition by U46619. Furthermore, SQ 29548 added after U46619 could restore channel activity to near control values. These results suggest that TxA2 could be a regulatory factor of KCa channels from coronary smooth muscle and that this regulation could be related to its action as a vasoconstrictor.

Oxygen free radical-mediated selective endothelial dysfunction in isolated coronary artery

1992 ◽  
Vol 262 (3) ◽  
pp. H806-H812 ◽  
Author(s):  
K. Todoki ◽  
E. Okabe ◽  
T. Kiyose ◽  
T. Sekishita ◽  
H. Ito
Keyword(s):  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Free Radicals ◽  
Free Radical ◽  
Coronary Artery ◽  
Iron Chelator ◽  
Oxygen Free Radical ◽  
Alpha Tocopherol ◽  
Endothelium Dependent Relaxation ◽  
Iron Chelator Deferoxamine

To understand the direct involvement of free radicals causing reduction in endothelium-dependent relaxation of isolated canine coronary ring preparations, this study was undertaken to examine the effect of free radicals generated from dihydroxy fumarate (DHF) plus Fe(3+)-ADP or from H2O2 plus FeSO4. The vasodilators (acetylcholine, bradykinin, A23187, and nitroglycerin) were given after DHF/Fe(3+)-ADP or H2O2/FeSO4 was removed from the organ chamber. The earlier DHF/Fe(3+)-ADP exposure produced an attenuation of the relaxation of the rings induced by acetylcholine, bradykinin, or A23187 but not of the relaxation induced by nitroglycerin. The observed effect of previous DHF/Fe(3+)-ADP exposure was significantly protected in the vessels isolated from the dogs treated with alpha-tocopherol. In the experiments for assessing the effect of various scavengers, 1O2 scavenger histidine or iron chelator deferoxamine effectively protected the attenuation induced by DHF/Fe(3+)-ADP exposure of the relaxation elicited by acetylcholine; superoxide dismutase (SOD), catalase, or dimethyl sulfoxide (DMSO) had no effect on this system. Furthermore, the relaxation elicited by acetylcholine, but not nitroglycerin, was significantly attenuated by the earlier exposure to .OH generated by Fenton's reagent (H2O2+FeSO4); the attenuation was significantly protected by DMSO. These results are consistent with the view that .OH, 1O2, and/or iron-dependent reactive species selectively damage endothelium-dependent relaxation as opposed to endothelium-independent relaxation in endothelium-intact coronary ring preparations. It is also postulated that lipid peroxidation may be responsible for this effect.

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