THE EFFECT OF CYCLOSPORINE ON THE RELEASE OF ENDOTHELIUM-DERIVED RELAXING FACTOR FROM ISOLATED HUMAN EPICARDIAL CORONARY ARTERIES

1991 ◽  
Vol 51 (3) ◽  
pp. 736-737 ◽  
Author(s):  
&NA;
Keyword(s):  
Coronary Arteries ◽  
Relaxing Factor ◽  
Endothelium Derived Relaxing Factor

Dietary omega 3 fatty acids and endothelium-dependent relaxations in porcine coronary arteries

1989 ◽  
Vol 256 (4) ◽  
pp. H968-H973 ◽  
Author(s):  
H. Shimokawa ◽  
P. M. Vanhoutte
Keyword(s):  
Fatty Acids ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Polyunsaturated Fatty Acids ◽  
Eicosapentaenoic Acid ◽  
Coronary Arteries ◽  
Treated Group ◽  
Omega 3 ◽  
Relaxing Factor ◽  
Endothelium Derived Relaxing Factor

Dietary supplementation with cod-liver oil significantly augments endothelium-dependent relaxations in porcine coronary arteries. The present study was designed to examine the effect of dietary administration of omega 3 polyunsaturated fatty acids (mainly eicosapentaenoic acid, the major component of fish oil) on endothelium-dependent relaxations in porcine coronary arteries. Male Yorkshire pigs were maintained 4 wk on a regular diet with or without supplementation with purified eicosapentaenoic acid (3.5 g/day) and docosahexaenoic acid (1.5 g/day). Endothelium-dependent relaxations were examined in vitro. In rings from the treated group, endothelium-dependent relaxations were augmented in response to bradykinin, serotonin, and ADP, but not to the calcium ionophore A23187. These augmentations were not altered by indomethacin but were significantly inhibited by methylene blue, an inhibitor of guanylate cyclase. In the treated group, endothelium-dependent relaxations to aggregating platelets also were significantly augmented; platelet-induced contractions of quiescent rings were inhibited more by the presence of the endothelium than in arteries from the control group. Bioassay experiments demonstrated that the release of endothelium-derived relaxing factor(s) by bradykinin and relaxations of the vascular smooth muscle to the factor(s) were greater in arteries from the treated group. These observations indicate that dietary omega 3 polyunsaturated fatty acids augment receptor-operated endothelium-dependent relaxations, partly due to the augmented release of endothelium-derived relaxing factor(s) and partly due to the augmented relaxation of the vascular smooth muscle to the factor(s).

Canine arteries release two different endothelium-derived relaxing factors

1989 ◽  
Vol 257 (1) ◽  
pp. H330-H333 ◽  
Author(s):  
U. Hoeffner ◽  
M. Feletou ◽  
N. A. Flavahan ◽  
P. M. Vanhoutte
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Coronary Artery ◽  
Vascular Smooth Muscle ◽  
Coronary Arteries ◽  
Relaxing Factor ◽  
Prostaglandin F2 Alpha ◽  
Donor Artery ◽  
Canine Coronary Artery ◽  
Endothelium Derived Relaxing Factor

Experiments were designed to analyze the effects of ouabain on the response of vascular smooth muscle to endothelium-derived relaxing factors released under basal conditions and on stimulation with acetylcholine or bradykinin. Bioassay rings of canine coronary artery (without endothelium) were superfused with perfusate from canine left circumflex coronary arteries with endothelium (donor arteries). During contractions of the bioassay ring evoked by prostaglandin F2 alpha, the relaxations caused by endothelium-derived relaxing factor(s), released under basal conditions or on exposure of the endothelial cells of the donor artery to maximally effective concentrations of acetylcholine, were reduced by incubation of the bioassay ring with ouabain. However, the relaxations evoked by infusion of bradykinin were not altered by incubation of the bioassay rings with ouabain. These experiments demonstrate the release of two endothelium-derived relaxing factors that can be distinguished using ouabain.

Cigarette smoke extract contracts isolated porcine coronary arteries by superoxide anion-mediated degradation of EDRF

1994 ◽  
Vol 266 (3) ◽  
pp. H874-H880 ◽  
Author(s):  
T. Murohara ◽  
K. Kugiyama ◽  
M. Ohgushi ◽  
S. Sugiyama ◽  
H. Yasue
Keyword(s):  
Methylene Blue ◽  
Cigarette Smoke ◽  
Coronary Arteries ◽  
Cigarette Smoke Extract ◽  
Isometric Tension ◽  
Relaxing Factor ◽  
Prostaglandin F2 Alpha ◽  
Endothelium Derived Relaxing Factor ◽  
Pig Coronary Arteries

To test whether cigarette smoke extract (CSE) influences the endothelial regulation of vascular tone in vitro, pig coronary arterial rings were incubated in organ chambers and isometric tension changes were examined. CSE was prepared by bubbling mainstream smoke of one filter cigarette into phosphate-buffered saline (2 ml). Fresh CSE (3.3, 10, and 30 microliters/ml) elicited initial contraction and subsequent relaxation during stable contraction to prostaglandin F2 alpha (PGF2 alpha). Initial contraction to CSE was dependent on the presence of endothelium, whereas subsequent relaxation was endothelium independent. Initial contraction was significantly attenuated by superoxide dismutase (SOD), methylene blue, but not by catalase. Prior inhibition of the basal release of endothelium-derived relaxing factor by NG-monomethyl-L-arginine also inhibited the initial contraction, and this inhibition was reversed by coincubation with L-arginine but not D-arginine. Subsequent relaxation was significantly potentiated by SOD but was markedly attenuated by methylene blue. CSE reduced ferricytochrome c, and this reduction was significantly inhibited by SOD. In conclusion, CSE induced biphasic tension change, initial contraction, and subsequent relaxation during stable contraction to PGF2 alpha in isolated pig coronary arteries. The initial contraction may be, at least in part, mediated through the degradation of basally released endothelium-derived relaxing factor (nitric oxide) by superoxide anions derived from CSE.

Conduit Coronary Artery: Control by Autonomic Nervous System

Physiology ◽  
1991 ◽  
Vol 6 (3) ◽  
pp. 103-107
Author(s):  
M Gerova
Keyword(s):  
Blood Flow ◽  
Nervous System ◽  
Smooth Muscle ◽  
Autonomic Nervous System ◽  
Coronary Artery ◽  
Coronary Arteries ◽  
Secondary Effect ◽  
Sympathetic Stimulation ◽  
Relaxing Factor ◽  
Endothelium Derived Relaxing Factor

Sympathetic stimulation induces a primary and secondary effect on smooth muscle of conduit coronary arteries. The former causes contraction, mediated by norepinephrine, and the latter, dilatation. The dilatation is due to endothelium-derived relaxing factor released as a consequence of the increased coronary blood flow.

Proximal and distal dog coronary arteries respond differently to basal EDRF but not to NO

1989 ◽  
Vol 256 (3) ◽  
pp. H828-H831 ◽  
Author(s):  
U. Hoeffner ◽  
C. Boulanger ◽  
P. M. Vanhoutte
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Coronary Artery ◽  
Sodium Nitroprusside ◽  
Coronary Arteries ◽  
Relaxing Factor ◽  
Prostaglandin F2 Alpha ◽  
Endothelium Derived Relaxing Factor

Experiments were designed to analyze the effects of endothelium-derived relaxing factor(s) (EDRF; released basally or on stimulation with acetylcholine) and nitric oxide (NO) on smooth muscle of coronary arteries of different diameter. During contractions of the bioassay ring evoked with prostaglandin F2 alpha, the relaxations caused by basal EDRF were greater in the distal than in the proximal coronary arteries, whereas there was no difference in response to the EDRF released by acetylcholine. During direct superfusion, NO caused similar relaxations in proximal and distal coronary artery rings. Optimal tension, prostaglandin F2 alpha-induced contractions, and relaxations caused by sodium nitroprusside were comparable in both preparations. In rings of proximal and distal coronary artery studied in organ chambers, acetylcholine caused comparable endothelium-dependent, whereas sodium nitroprusside and NO cause comparable endothelium-independent relaxations. These experiments indicate a difference in response of different-sized coronary arteries to basally released EDRF and suggest that the basally released factor differs from NO.

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