Modification by LY 83583 and methylene blue of relaxation induced by nitric oxide, glyceryl trinitrate, sodium nitroprusside and atriopeptin in aortae of the rat, guinea-pig and rabbit

1994 ◽  
Vol 25 (7) ◽  
pp. 1361-1371 ◽  
Author(s):  
Tomie Kawada ◽  
Takaharu Ishibashi ◽  
Hiroki Sasage ◽  
Kiminori Kato ◽  
Shoichi Imai
Keyword(s):  
Nitric Oxide ◽  
Methylene Blue ◽  
Guinea Pig ◽  
Glyceryl Trinitrate ◽  
Sodium Nitroprusside ◽  
Ly 83583

Is nitric oxide the only endothelium-derived relaxing factor in canine femoral veins?

1989 ◽  
Vol 257 (6) ◽  
pp. H1910-H1916 ◽  
Author(s):  
V. M. Miller ◽  
P. M. Vanhoutte
Keyword(s):  
Nitric Oxide ◽  
Methylene Blue ◽  
Superoxide Dismutase ◽  
Sodium Nitroprusside ◽  
Femoral Vein ◽  
Pulmonary Veins ◽  
Chemical Properties ◽  
Relaxing Factor ◽  
Endothelium Derived Relaxing Factor ◽  
Ly 83583

Nitric oxide may be an endothelium-derived relaxing factor in systemic arteries and pulmonary veins. The endothelium-derived relaxing factor of systemic veins has not been characterized. Experiments were designed to determine whether the endothelium-derived relaxing factor of systemic veins shared chemical properties and mechanisms of action with nitric oxide. Rings of the canine femoral vein with and without endothelium were suspended in organ chambers for the measurement of isometric force. In rings without endothelium, relaxations to nitric oxide were augmented by superoxide dismutase plus catalase and were inhibited by hemoglobin, methylene blue, and LY 83583. The endothelium-dependent relaxations to acetylcholine and A23187 were not augmented by superoxide dismutase plus catalase but were inhibited by hemoglobin and only moderately reduced by either methylene blue or LY 83583. Relaxations to sodium nitroprusside were not inhibited by methylene blue and LY 83583. Relaxations to sodium nitroprusside were inhibited by ouabain and K+-free solution; those to nitric oxide were not. These results indicate that although the endothelium-derived relaxing factor released from canine systemic veins shares some chemical properties with nitric oxide, the mechanism by which relaxations are induced by the two differ. A factor dissimilar to nitric oxide but acting like sodium nitroprusside may be released by the endothelium of canine systemic veins.

Modulation of vasoactive intestinal peptide pulmonary relaxation by NO in tracheally superfused guinea pig lungs

1993 ◽  
Vol 265 (4) ◽  
pp. L410-L415 ◽  
Author(s):  
C. M. Lilly ◽  
J. S. Stamler ◽  
B. Gaston ◽  
C. Meckel ◽  
J. Loscalzo ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Methylene Blue ◽  
Confidence Interval ◽  
Guinea Pig ◽  
Vasoactive Intestinal Peptide ◽  
Inhibitory Effect ◽  
Lung Perfusion ◽  
Perfusion Fluid ◽  
Oxide Synthase ◽  
Dependent Mechanism

The mechanism of vasoactive intestinal peptide (VIP)-induced pulmonary relaxation in tracheally perfused guinea pig lungs was defined with the use of inhibitors of nitric oxide synthase (NOS) and by direct measurement of nitric oxide (NO) equivalents recovered from lung perfusion fluid. Lungs treated with 200 microM NG-nitro-L-arginine were resistant to the relaxant effects of VIP in these lungs; the 50% inhibitory dose (ID50) for VIP was 32 nmol/kg (95% confidence interval, 16–79), which was approximately 100-fold greater than the ID50 of control lungs which was 0.39 nmol/kg, (0.16–0.79, P < 0.0001). This inhibitory effect could be overcome with excess L- but not D-arginine. In contrast, VIP-induced relaxation of isolated guinea pig trachea was not modified by inhibitors of NOS. To confirm that VIP infusion resulted in NO generation in whole lungs, we measured NO equivalents in lung effluent by two distinct technologies. We found that VIP injection caused a significant increase in NO equivalents from 0.11 +/- 0.04 microM to 0.78 +/- 0.15 microM (P < 0.05) and that this increase preceded VIP-induced pulmonary relaxation. Lungs pretreated with the putative guanylyl cyclase inhibitor methylene blue were less responsive to VIP [ID50 4.0 nmol/kg (1.5–10), P < 0.005 compared with control lungs], consistent with a physiologically significant guanosine 3',5'-cyclic monophosphate-dependent mechanism. Our data demonstrate that VIP has the capacity to relax whole lungs in part by stimulating the generation of NO.

scholarly journals Effects of cGMP and the nitric oxide donors glyceryl trinitrate and sodium nitroprusside on contractions in vitro of isolated myometrial tissue from pregnant women

Reproduction ◽  
1997 ◽  
Vol 110 (2) ◽  
pp. 249-254 ◽  
Author(s):  
J. E. Norman ◽  
L. M. Ward ◽  
W. Martin ◽  
A. D. Cameron ◽  
J. C. McGrath ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Glyceryl Trinitrate ◽  
Pregnant Women ◽  
Sodium Nitroprusside ◽  
Nitric Oxide Donors

Endogenous vasodilators modulate pulmonary vascular anaphylaxis

1994 ◽  
Vol 76 (2) ◽  
pp. 916-922 ◽  
Author(s):  
L. J. Kelly ◽  
B. J. Undem ◽  
G. K. Adams
Keyword(s):  
Nitric Oxide ◽  
Methylene Blue ◽  
Methyl Ester ◽  
Guinea Pig ◽  
Initial Phase ◽  
Contractile Response ◽  
Pulmonary Arteries ◽  
Relaxing Factor ◽  
Anaphylactic Contraction

We examined the role of endothelium-derived nitric oxide during antigen-induced contraction in pulmonary arteries isolated from actively sensitized guinea pigs. Ovalbumin (10(-2) mg/ml)-induced contraction was not sustained, and tension returned to baseline within 15 min. Pretreatment with methylene blue (10(-5) M) increased both the amplitude and the duration of the contractile response in these tissues. At 15 min, tension remained elevated and was > 70% of the peak amplitude. Removal of the endothelium with saponin (200 micrograms/ml) increased the magnitude of the contraction by > 125%; however, the duration of the response was unaffected. After pretreatment with saponin, methylene blue no longer increased the amplitude of antigen-induced contraction but its effect on the duration was unchanged. Pretreatment with nitro-L-arginine methyl ester significantly increased the magnitude of the contraction in each of the tissues. These results suggest that the response of guinea pig pulmonary arteries to antigen is modulated by two types of endogenous vasodilators, endothelium-derived nitric oxide that inhibits the initial phase of the response and an endothelium-independent relaxing factor that is guanosine 3′,5′-cyclic monophosphate dependent and attenuates the duration of anaphylactic contraction.

Actions of nitric oxide-generating sodium nitroprusside in myenteric plexus of guinea pig small intestine

1993 ◽  
Vol 265 (5) ◽  
pp. G887-G893 ◽  
Author(s):  
K. Tamura ◽  
M. Schemann ◽  
J. D. Wood
Keyword(s):  
Nitric Oxide ◽  
Small Intestine ◽  
Guinea Pig ◽  
Sodium Nitroprusside ◽  
Myenteric Plexus ◽  
Membrane Properties ◽  
Dependent Manner ◽  
Membrane Excitability ◽  
Concentration Dependent Manner ◽  
Myenteric Neurons

Sodium nitroprusside (NaNP) was used as a donor of nitric oxide (NO) to investigate actions of NO on electrical and synaptic behavior of single myenteric neurons in guinea pig small intestine. NaNP (10 microM-1 mM) did not affect resting membrane properties of the neurons, except for an occasional decrease in input resistance and hyperpolarization attributable to suppression of excitatory transmitter release. NaNP did not alter fast nicotinic neurotransmission but suppressed noncholinergic slow excitatory postsynaptic potentials (slow EPSPs) in a concentration-dependent manner. Pretreatment with either methylene blue or oxyhemoglobin reduced the inhibitory action of NaNP on the slow EPSPs. Slow EPSP-like responses to microejected substance P or 5-hydroxytryptamine were unaffected by NaNP. The nitric oxide synthase inhibitor, N omega-nitro-L-arginine methyl ester, did not affect resting membrane excitability or excitatory synaptic events in any of the myenteric neurons. The results suggest that NO may not be released extensively as a neurotransmitter at synapses within the myenteric plexus. If myenteric neurons are exposed to NO released from nonneural sources, then the principal action is expected to be presynaptic inhibition of slow synaptic excitation.

Differential effects of nitrovasodilators and nitric oxide on porcine tracheal and bronchial muscle in vitro

1994 ◽  
Vol 77 (3) ◽  
pp. 1142-1147 ◽  
Author(s):  
K. Stuart-Smith ◽  
T. C. Bynoe ◽  
K. S. Lindeman ◽  
C. A. Hirshman
Keyword(s):  
Nitric Oxide ◽  
Methylene Blue ◽  
Smooth Muscle ◽  
Sodium Nitroprusside ◽  
Airway Smooth Muscle ◽  
Muscle Relaxation ◽  
Ringer Solution ◽  
Smooth Muscle Relaxation ◽  
Response Curves

Nitrovasodilators and nitric oxide relax airway smooth muscle. The mechanism by which nitrovasodilators are thought to act is by release of nitric oxide, but the importance of nitric oxide in nitrovasodilator-induced airway smooth muscle relaxation is unclear. The aim of this study was to compare the relaxing effects of nitric oxide itself with those of nitrovasodilators in porcine tracheal muscle and intrapulmonary airways and to investigate the mechanisms involved. Strips of porcine tracheal smooth muscle, rings of bronchi, and strips of bronchi from the same animal were suspended in organ chambers in modified Krebs Ringer solution (95% O2–5% CO2, 37 degrees C). Tissues were contracted with carbachol, and concentration-response curves to nitric oxide, sodium nitroprusside, and SIN-1 (an active metabolite of molsidomine) were obtained. All tissues relaxed to sodium nitroprusside, SIN-1, and nitric oxide. The relaxation to nitric oxide but not to SIN-1 or sodium nitroprusside was inhibited by methylene blue. Tissues pretreated with methylene blue that failed to relax to nitric oxide were, however, relaxed by sodium nitroprusside. These results demonstrate that nitrovasodilators relax airways by a mechanism other than by or in addition to the release of nitric oxide.

Etomidate and Thiopental Inhibit the Release of Endothelium-derived Hyperpolarizing Factor in the Human Renal Artery

1996 ◽  
Vol 84 (6) ◽  
pp. 1485-1488 ◽  
Author(s):  
Paul Kessler ◽  
Volker Lischke ◽  
Markus Hecker
Keyword(s):  
Nitric Oxide ◽  
Cytochrome P450 ◽  
Nitric Oxide Synthase ◽  
Renal Artery ◽  
Glyceryl Trinitrate ◽  
Sodium Nitroprusside ◽  
Ca Channel ◽  
Intravenous Anesthetics ◽  
Relaxant Response ◽  
Oxide Synthase

Background Endothelium-derived hyperpolarizing factor is thought to be a cytochrome P450-derived arachidonic acid metabolite that hyperpolarizes vascular smooth muscle cells by opening Ca(2+)-activated K+ channels (K+Ca channels). In the rabbit carotid artery both volatile and intravenous anesthetics inhibit the acetylcholine-stimulated release of endothelium-derived hyperpolarizing factor. Because the release of this factor may help to maintain vascular tone in humans under conditions of a failing nitric oxide synthesis, e.g., in atherosclerosis, the effects of two intravenous anesthetics, thiopental and etomidate, on the endothelium-derived hyperpolarizing factor-mediated relaxant response to acetylcholine were investigated in human isolated renal artery segments. Methods The segments were suspended in Krebs-Henseleit solution (37 degrees C) containing the cyclooxygenase inhibitor diclofenac (1 microM) and preconstricted with norepinephrine (6 microM). Relaxations caused by acetylcholine (1 microM) were compared in the presence and absence of the nitric oxide synthase inhibitor N(G)-nitro-L-arginine (0.1 mM) in control segments and in segments exposed to etomidate or thiopental (0.03-0.3 mM). In addition, the effects of the two anesthetics on the relaxant response to the nitric oxide donors glyceryl trinitrate (3 microM) and sodium nitroprusside (0.1 microM) were examined. Results The relaxant response to acetylcholine, which was resistant to both nitric oxide synthase and cyclooxygenase blockade, was markedly reduced by the K+Ca channel antagonist tetrabutyl ammonium (3 mM) and the cytochrome P450 inhibitor clotrimazole (30 microM). Both etomidate and thiopental, at a concentration of 0.3 mM, selectively attenuated the relaxant response to acetylcholine in N(G)-nitro-L-arginine-treated segments, but did not affect relaxations elicited by glyceryl trinitrate or sodium nitroprusside. Conclusions Etomidate and thiopental inhibit the endothelium-derived hyperpolarizing factor-mediated relaxant response to acetylcholine in the human renal artery, an effect that appears to be attributable to the cytochrome P450-inhibiting properties of these anesthetics.

scholarly journals Relaxation of guinea-pig trachea by sodium nitroprusside: cyclic GMP and nitric oxide not involved

1996 ◽  
Vol 118 (3) ◽  
pp. 466-470 ◽  
Author(s):  
Gudarz Sadeghi-Hashjin ◽  
Gert Folkerts ◽  
Paul A.J. Henricks ◽  
Peet G.F. Loo ◽  
Ilse E.M. Dik ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Guinea Pig ◽  
Sodium Nitroprusside ◽  
Cyclic Gmp

Inhibition of nitrovasodilators by pyocyanin and methylene blue is dissociated from nitric oxide formation

1994 ◽  
Vol 72 (7) ◽  
pp. 746-752 ◽  
Author(s):  
Jovan Bozinovski ◽  
James F. Brien ◽  
Gerald S. Marks ◽  
Kanji Nakatsu
Keyword(s):  
Nitric Oxide ◽  
Methylene Blue ◽  
Sodium Nitroprusside ◽  
Isosorbide Dinitrate ◽  
Rabbit Aorta ◽  
Aortic Ring ◽  
Organic Nitrates ◽  
No Production ◽  
Nitric Oxide Formation ◽  
No Formation

The phenazine pigment pyocyanin (Pyo), like methylene blue (MB), inhibits vascular relaxation induced by organic nitrates. These nitrovasodilators are pro-drugs that have in common the ability to generate nitric oxide (NO). In this study, we characterized responses of rabbit isolated aortic ring to 3-morpholinosydnonimine (SIN-1), S-nitroso-N-acetylpenicillamine (SNAP), sodium nitroprusside, glyceryl trinitrate (GTN), and isosorbide dinitrate in the presence and absence of 10 μM Pyo. We also examined the effect of Pyo (1 and 10 μM) and MB (1 and 10 μM) on vasorelaxation induced by authentic NO, and finally we tested the effects of Pyo and MB on the tissue-independent formation of NO from SIN-1, SNAP, and sodium nitroprusside, using die chemiluminescence – headspace gas method. Pyo (10 μM) surmountably inhibited aortic responses to GTN, isosorbide dinitrate, SIN-1, and SNAP with a characteristic rightward shift of the dose–response curve; the apparent EC50 of these drugs for relaxation of phenylephrine-contracted aorta was increased 18-, 4-, 13-, and 15-fold, respectively. Pyo (1 and 10 μM) and MB (10 μM) inhibited NO-induced vasorelaxation at the EC50 of NO by 35, 72, and 56%. In contrast, Pyo did not inhibit sodium nitroprusside induced vasodilation. For a 10-min incubation, 10 μM Pyo or MB increased NO production from SNAP 1.8- and 2.9-fold, respectively, and increased NO production from SIN-1 by 3.8- and 7.1-fold, respectively. Neither Pyo nor MB enhanced NO formation from sodium nitroprusside. These data indicate that Pyo and MB inhibit nitrovasodilator-induced relaxation of aortic ring by interfering with the action of NO, subsequent to its formation.Key words: pyocyanin, nitric oxide, methylene blue, nitrovasodilators, rabbit aorta.

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