scholarly journals Differential selectivity of endothelium-derived relaxing factor and nitric oxide in smooth muscle

1987 ◽  
Vol 92 (3) ◽  
pp. 483-485 ◽  
Author(s):  
Kazuhisa Shikano ◽  
Eliot H. Ohlstein ◽  
Barry A. Berkowitz
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Relaxing Factor ◽  
Endothelium Derived Relaxing Factor ◽  
Differential Selectivity

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.

Differential sensitivity to endothelin in canine arteries and veins

1989 ◽  
Vol 257 (4) ◽  
pp. H1127-H1131 ◽  
Author(s):  
V. M. Miller ◽  
K. Komori ◽  
J. C. Burnett ◽  
P. M. Vanhoutte
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Mesenteric Arteries ◽  
Differential Sensitivity ◽  
Ionophore A23187 ◽  
Arterial Smooth Muscle ◽  
Relaxing Factor ◽  
Saphenous Veins ◽  
Endothelium Derived Relaxing Factor ◽  
Arteries And Veins

Experiments were designed to compare the sensitivity of venous and arterial smooth muscle to endothelin and to determine whether contractions to the peptide could be inhibited by endothelium-derived relaxing factor and nitric oxide. Rings of canine left anterior descending coronary, femoral, and mesenteric arteries and femoral and saphenous veins with and without endothelium were suspended for measurement of isometric force. In the presence of indomethacin, phentolamine, and propranolol, endothelin initiated concentration-dependent increases in tension in all rings. The veins were more sensitive to the peptide than were the arteries. Endothelin depolarized the smooth muscle of the saphenous veins and mesenteric arteries; the threshold concentration for depolarization was approximately 100 times lower in the veins (10(-10) M) than in the arteries (10(-8) M). Removal of the endothelium enhanced the sensitivity only of venous smooth muscle to endothelin. However, stimulation of the endothelium in the arteries with either acetylcholine or the calcium ionophore A23187 rapidly inhibited the maximal tension developed to the peptide. Nitric oxide inhibited contractions to endothelin in arteries and veins without endothelium; the inhibition was greater in the arteries than in the veins. These results indicate that venous smooth muscle is more sensitive than arterial smooth muscle to endothelin. In both blood vessels, endothelium-derived relaxing factor(s) can inhibit contractions to the peptide.

Role of 11,12,15-Trihydroxyeicosatrienoic Acid as a New Endothelium-Derived Relaxing Factor

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 678-678
Author(s):  
Kathryn M Gauthier ◽  
Sandra L Pfister ◽  
Nancy Spitzbarth ◽  
Nancy J Rusch ◽  
William B Campbell
Keyword(s):  
Nitric Oxide ◽  
Arachidonic Acid ◽  
Smooth Muscle ◽  
Rabbit Aorta ◽  
Channel Blockers ◽  
Lipoxygenase Inhibitor ◽  
Lipoxygenase Product ◽  
Relaxing Factor ◽  
Endothelium Derived Relaxing Factor ◽  
Mass Spectometry

3 The endothelium regulates vascular tone through the release of relaxing factors including nitric oxide, prostacyclin, epoxyeicosatrienoic acids and others not yet identified. The purpose of this study was to characterize the 15-lipoxygenase product, 11,12,15-trihydroxyeicosatrienoic acid (11,12,15-THETA), as a new endothelial relaxing factor. In phenylephrine-constricted rabbit aorta, acetylcholine induced a dose-dependent relaxation in the presence of cyclooxygenase blockade with indomethicin (10 μM) and nitric oxide blockade with nitro-arginine (30 μM) which was eliminated by pretreatment with cinnamyl-3,4,-dihydroxy-a-cyanocinnamate (CDC)(1 μM) a specific lipoxygenase inhibitor, and miconizole (1 μM) a cytochrome P450 inhibitor. Additionally, arachidonic acid (1 nM - 10 μM) relaxed precontracted rabbit aorta, and this relaxation was maximally inhibited by 50% either by increasing the potassium (K + ) concentration from 4 mM to 20 mM or by the addition of the K + channel blockers, apamin (100 nM) plus charybdotoxin (100 nM). In patch-clamp studies of inside-out patches of rabbit aortic smooth muscle, we have identified a 20 pS K + channel, which is activated by increased calcium concentrations and blocked by apamin (1 μM). Structural analysis of arachidonic acid metabolites from rabbit aorta by gas chromatography/mass spectometry has revealed two 15-lipoxygenase product regioisomers; 11,12,15-THETA and 11,14,15-THETA. The synthesis of these metabolites was inhibited by CDC and miconizole. The addition of the 11,12,15-THETA fraction to precontracted rabbit aorta resulted in a concentration-dependent relaxation, which was blocked by elevated K + . The other regioisomer was without effect. These results suggest that 11,12,15-THETA, a 15-lipoxygenase metabolite, represents a novel endothelium-derived relaxing factor, which induces relaxation possibly through the activation of apamin-sensitive K + channels located in the vascular smooth muscle.

Modulation of cerebral arterial tone by endothelium-derived relaxing factor

1993 ◽  
Vol 264 (4) ◽  
pp. H1245-H1250 ◽  
Author(s):  
J. E. Brian ◽  
R. H. Kennedy
Keyword(s):  
Nitric Oxide ◽  
Muscle Tone ◽  
Cerebral Arteries ◽  
Maximum Tension ◽  
Relaxing Factor ◽  
Middle Cerebral Arteries ◽  
Endothelium Derived Relaxing Factor ◽  
Vascular Smooth Muscle Tone ◽  
Dose Dependent ◽  
Arterial Tone

This study was designed to further elucidate the role of the endothelium in regulation of cerebral vascular smooth muscle tone. Dose-dependent vasoconstrictive effects of serotonin (5-HT) were examined in endothelium-intact and endothelium-denuded ring segments prepared from canine basilar and middle cerebral arteries. Some preparations were pretreated with 10(-5) M N omega-nitro-L-arginine (L-NNA), an agent that inhibits the production of L-arginine-derived nitric oxide, one of the compounds proposed to be endothelium-derived relaxing factor. L-NNA alone elicited marked dose-dependent increases in tension in endothelium-intact preparations; a significantly smaller response was seen in endothelium-denuded preparations. The effects of L-NNA on endothelium-intact preparations were partially reversed by washing and treatment with L-arginine. The maximum tension induced by 5-HT was approximately doubled by removal of the endothelium as well as by L-NNA treatment of endothelium-intact preparations; a slight increase in maximum tension occurred in endothelium-denuded preparations treated with L-NNA. The concentration of 5-HT producing half-maximal contraction (ED50) was not affected by L-NNA. These data suggest that L-arginine-derived nitric oxide modulates canine cerebral arterial tone in both the resting state and during contraction with 5-HT.

Endothelial Dysfunction in Shock States

Physiology ◽  
1993 ◽  
Vol 8 (4) ◽  
pp. 145-148 ◽  
Author(s):  
AGB Kovach ◽  
AM Lefer
Keyword(s):  
Nitric Oxide ◽  
Endothelial Dysfunction ◽  
Tissue Injury ◽  
Circulatory Shock ◽  
Relaxing Factor ◽  
Vascular Beds ◽  
Endothelium Derived Relaxing Factor

Circulatory shock results in dysfunction of the endothelium in various vascular beds. This dysfunction is characterized by marked impairment in the vasculature's ability to relax to endothelium-dependent vasodilators. This loss of endothelium-derived relaxing factor, or nitric oxide, leads to profound tissue injury.

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