Different Involvement of Endothelium-Derived Relaxing Factor and Prostacyclin in Vasodilator Response to Bradykinin in Isolated Dog Blood Vessels

1989 ◽  
pp. 429-434 ◽  
Author(s):  
Tomio Okamura ◽  
Noboru Toda
Keyword(s):  
Blood Vessels ◽  
Vasodilator Response ◽  
Relaxing Factor ◽  
Dog Blood ◽  
Endothelium Derived Relaxing Factor

Endotoxin-induced alterations in contractility of isolated blood vessels from sheep

1991 ◽  
Vol 260 (6) ◽  
pp. H1790-H1794 ◽  
Author(s):  
S. Nelson ◽  
R. H. Steward ◽  
L. Traber ◽  
D. Traber
Keyword(s):  
Escherichia Coli ◽  
Cardiac Output ◽  
Pulmonary Artery ◽  
Blood Vessels ◽  
Femoral Artery ◽  
Vascular Reactivity ◽  
Relaxing Factor ◽  
Tertiary Branch ◽  
Endothelium Derived Relaxing Factor ◽  
And Control

The present study examined reactivity to norepinephrine (NE) and KCl in isolated, suffused blood vessels from the systemic and pulmonary circulations of endotoxin-treated and control sheep. A possible mechanism underlying an endotoxin-induced alteration in vascular reactivity was also investigated. Chronically instrumented sheep were given Escherichia coli endotoxin (1.5 micrograms/kg). Eight to 12 h later these endotoxin-treated animals exhibited a significantly increased cardiac output and decreased systemic vascular pressure and resistance. The pulmonary vascular pressure and resistance were not changed. The isolated superficial femoral artery from the endotoxin sheep exhibited depressed contractions in response to KCl (75 mM) and to NE (10(-7)-10(-5) M), whereas the pulmonary artery (tertiary branch) did not exhibit altered reactivity. The decreased sensitivity to NE in the femoral artery from endotoxin sheep did not appear to involve an alteration of alpha- or beta-adrenoceptors, or an increased release of vasodilator prostanoids, or endothelium-derived relaxing factor.

N omega-nitro-L-arginine and pulmonary vascular pressure-flow relationship in conscious dogs

1992 ◽  
Vol 262 (5) ◽  
pp. H1331-H1337 ◽  
Author(s):  
K. Nishiwaki ◽  
D. P. Nyhan ◽  
P. Rock ◽  
P. M. Desai ◽  
W. P. Peterson ◽  
...  
Keyword(s):  
Conscious Dogs ◽  
Vasomotor Tone ◽  
Dose Response Relationship ◽  
Pressure Flow ◽  
Vasodilator Response ◽  
Relaxing Factor ◽  
Pulmonary Vasoconstriction ◽  
Pulmonary Vasodilator ◽  
Endothelium Derived Relaxing Factor ◽  
Endogenous Release

We investigated the effects of an inhibitor of nitric oxide (NO) synthesis, N omega-nitro-L-arginine (L-NNA), on the pulmonary vascular pressure-flow relationship in chronically instrumented conscious dogs. The L-arginine analogue L-NNA (20 mg/min for 60 min iv) had no effect on the baseline pressure-flow relationship. This result indicates that tonic release of endothelium-derived relaxing factor (EDRF), which is thought to be NO or a labile NO-generating molecule, is not responsible for low resting pulmonary vasomotor tone in conscious dogs. In contrast, L-NNA caused a leftward shift in the dose-response relationship to the thromboxane mimetic U-46619, indicating that the endogenous release of EDRF modulates the pulmonary vascular response to this vasoconstrictor. Finally, after preconstriction with U-46619, L-NNA abolished the pulmonary vasodilator response to bradykinin (1-10 micrograms.kg-1.min-1) but had no effect on the pulmonary vasodilator response to sodium nitroprusside (1-10 micrograms.kg-1.min-1). Thus EDRF does not appear to tonically regulate the baseline pulmonary vascular pressure-flow relationship in conscious dogs. However, EDRF does act to attenuate the magnitude of U-46619-induced pulmonary vasoconstriction. Moreover, the pulmonary vasodilator response to bradykinin is entirely mediated by EDRF in conscious dogs.

Anti-EDRF effect of tumor necrosis factor in isolated, perfused cat carotid arteries

1989 ◽  
Vol 256 (5) ◽  
pp. H1509-H1512 ◽  
Author(s):  
N. Aoki ◽  
M. Siegfried ◽  
A. M. Lefer
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Carotid Arteries ◽  
Human Tumor ◽  
Vasodilator Response ◽  
Relaxing Factor ◽  
Endothelium Derived Relaxing Factor ◽  
Inhibitor Of Protein Synthesis ◽  
Necrosis Factor ◽  
Factor Release

Cat carotid arteries that have an intact endothelium were isolated and perfused with Krebs-Henseleit solution containing recombinant human tumor necrosis factor (rhTNF). Perfused arteries were preconstricted with KCl and then dilated with acetylcholine (ACh) or acidified NaNO2. After perfusion with TNF (4 micrograms/ml) for 120 min, the ACh-induced vasodilator response was markedly blunted, but the NaNO2 vasodilator response was not significantly affected. Arteries perfused with 2 micrograms/ml TNF for 60-120 min or with 4 micrograms/ml for 60 min did not develop a significantly impaired relaxation to ACh. Moreover, perfusion with 20-100 micrograms/ml cycloheximide, an inhibitor of protein synthesis, blocked the TNF-induced impairment of the relaxation to ACh. On the other hand, the vasodilator response to acidified NaNO2 did not change in any perfused carotid arteries. These results suggest that TNF promotes the synthesis of proteins that contribute to the damage of endothelial cells directly, probably by inhibiting endothelium-derived relaxing factor release.

scholarly journals EVIDENCE FOR THE PRESENCE OF ENDOTHELIUM-DERIVED RELAXING FACTOR IN NASAL BLOOD VESSELS

1993 ◽  
Vol 96 (5) ◽  
pp. 761-766,871
Author(s):  
WATARU OKITA ◽  
TOSHIYOSHI TANAKA ◽  
TOSHITAKA IINUMA ◽  
KEIICHI ICHIMURA
Keyword(s):  
Blood Vessels ◽  
Relaxing Factor ◽  
Endothelium Derived Relaxing Factor ◽  
Nasal Blood Vessels

Inhibition by arachidonate of cerebral arteriolar dilation from acetylcholine

1989 ◽  
Vol 256 (3) ◽  
pp. H665-H671 ◽  
Author(s):  
H. A. Kontos ◽  
E. P. Wei ◽  
J. T. Povlishock ◽  
R. C. Kukreja ◽  
M. L. Hess
Keyword(s):  
Superoxide Dismutase ◽  
Hydroxyl Radical ◽  
Topical Application ◽  
The Other ◽  
Cranial Window ◽  
Vasodilator Response ◽  
Relaxing Factor ◽  
Brain Surface ◽  
Endothelium Derived Relaxing Factor ◽  
The Brain

After topical application of arachidonate (200 micrograms/ml) on the brain surface of anesthetized cats equipped with cranial windows, the vasodilator response to topical acetylcholine (10(-7) M) was either abolished or converted to vasoconstriction. This effect of arachidonate was prevented by pretreatment with topical deferoxamine (1 mM) to chelate free iron and inhibit the generation of hydroxyl radical from the Haber-Weiss reaction. Posttreatment with deferoxamine or with the combination of superoxide dismutase and catalase did not reestablish the vasodilator response to acetylcholine. Using a bioassay preparation in which one cranial window served as the donor for endothelium-derived relaxing factor (EDRF) while the other window was used to assay EDRF, we found that arachidonate applied to the donor window inhibited the generation and/or release of EDRF. Arachidonate applied to the assay window did not influence the response to EDRF. The results show that arachidonate interferes with the vasodilator response to acetylcholine, primarily because it inhibits the generation and release of EDRF. This effect is caused by injury to the endothelium induced by hydroxyl radical.

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