Comparison of relaxation responses of vascular and non-vascular smooth muscle to endothelium-derived relaxing factor (EDRF), acidified sodium nitrite (NO) and sodium nitroprusside

1990 ◽  
Vol 341 (4) ◽  
Author(s):  
T.M. Cocks ◽  
J.A. Angus
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Sodium Nitroprusside ◽  
Sodium Nitrite ◽  
Relaxing Factor ◽  
Endothelium Derived Relaxing Factor ◽  
Relaxation Responses

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.

Inhibition of the acetylcholine-induced relaxation of canine isolated basilar artery by potassium-conductance blockers

1991 ◽  
Vol 69 (6) ◽  
pp. 786-791 ◽  
Author(s):  
D. A. Elliott ◽  
M. Gu ◽  
B. Y. Ong ◽  
D. Bose
Keyword(s):  
Smooth Muscle ◽  
Sodium Nitroprusside ◽  
Basilar Artery ◽  
Sodium Pump ◽  
Potassium Conductance ◽  
K Channel ◽  
Relaxing Factor ◽  
Mechanical Removal ◽  
Canine Basilar Artery ◽  
Endothelium Derived Relaxing Factor

Canine basilar artery rings precontracted with 5-hydroxytryptamine (0.1–0.5 μM) relaxed in the presence of acetylcholine (25–100 μM), sodium nitroprusside (0.1 μM), or stimulation of the electrogenic sodium pump by restoration of extracellular K+ (4.5 mM) after K+- deprivation. Acetylcholine-induced relaxation is believed to be caused by the release of endothelium-derived relaxing factor (EDRF) and is prevented by mechanical removal of the endothelium, while relaxations induced by sodium nitroprusside or restarting of the sodium pump are endothelium-independent. Acetylcholine-induced relaxation was selectively blocked by pretreatment of the tissue with the nonselective K+ conductance inhibitors, 4-aminopyridine (4-AP, 3 mM), Ba2+ (1 mM), and tetraethylammonium (20 mM). 4-AP also blocked ACh-mediated relaxation in muscles contracted with elevated external K+. Relaxation of 5-hydroxytryptamine-induced contraction by sodium nitroprusside, or by addition of K+ to K+-deprived muscle, was not affected by 4-AP. Relaxation of basilar artery with acidified sodium nitrite solution (containing nitric oxide) was reduced by 4-AP. These results suggest that 4-AP and possibly Ba2+ inhibit acetylcholine-induced endothelium-dependent relaxation by inhibition of the action of EDRF on the smooth muscle rather than through inhibition of release of EDRF. The increase in K+ conductance involved in acetylcholine-induced relaxation is not due to ATP-inhibited K+ channels, as it is not blocked by glyburide (10−6 M). Endothelium-derived relaxant factor(s) may relax smooth muscle by mode(s) of action different from that of sodium nitroprusside or by hyperpolarization due to the electrogenic sodium pumping. Since 4-AP and similar agents are used to increase myogenic tone, the absence of the endothelium may be mistakenly assumed in the presence of these agents.Key words: Ba2+, blood vessels, endothelium-derived hyperpolarizing factor, endothelium-derived relaxing factor, glyburide, K channel, pinacidil, relaxation.

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.

Impairment of endothelium-dependent relaxation of superior mesenteric artery in genetically diabetic WBN/Kob rats

1993 ◽  
Vol 71 (3-4) ◽  
pp. 297-300 ◽  
Author(s):  
Noriyuki Miyata ◽  
Hiroko Yamaura ◽  
Katsuharu Tsuchida ◽  
Shigeru Okuyama ◽  
Susumu Otomo ◽  
...  
Keyword(s):  
Sodium Nitroprusside ◽  
Superior Mesenteric Artery ◽  
Mesenteric Artery ◽  
Wistar Rats ◽  
Diabetic Rats ◽  
Mesenteric Arteries ◽  
Relaxing Factor ◽  
Endothelium Derived Relaxing Factor ◽  
Relaxation Responses ◽  
Endothelium Dependent Relaxation

The endothelium-dependent relaxation of superior mesenteric arteries of Wistar and genetically diabetic WBN/Kob rats was compared. Endothelium-dependent relaxation induced by acetylcholine (ACh) and A23187 was depressed in WBN/Kob rats. Relaxation induced by sodium nitroprusside, an endothelium-independent agent, in strips from WBN/Kob rats was similar to that in strips from Wistar rats. Indomethacin (5 × 10−6 M) enhanced the relaxation responses to ACh in strips from both WBN/Kob and Wistar rats; however, endothelium-dependent relaxation induced by ACh remained attenuated in WBN/Kob rats. These results show that endothelium-dependent relaxation is impaired not only in thoracic aorta but also in superior mesenteric arteries in genetically diabetic rats.Key words: acetylcholine, A23187, sodium nitroprusside, indomethacin, genetically diabetic rats, endothelium-derived relaxing factor.

Endothelium-Derived Relaxing Factor: In Search of the Endogenous Nitroglycerin

Physiology ◽  
1987 ◽  
Vol 2 (2) ◽  
pp. 61-64
Author(s):  
I Fridovich ◽  
P-O Hagen ◽  
JJ Murray
Keyword(s):  
Smooth Muscle ◽  
Platelet Aggregation ◽  
Vascular Smooth Muscle ◽  
Vascular Endothelium ◽  
Inhibitory Activity ◽  
Chemical Stabilization ◽  
Relaxing Factor ◽  
Physiological Regulator ◽  
Endothelium Derived Relaxing Factor

A mediator released from vascular endothelium is characterized by a potent relaxing activity on vascular smooth muscle as well as an inhibitory activity on platelet aggregation. It is distinctly different from prostacyclin and is referred to as endothelial-derived relaxing factor or EDRF. It is extremely labile, but the recent chemical stabilization of the elusive factor should help unravel its identity and define the activity of this important physiological regulator.

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