Methylene blue inhibits coronary arterial relaxation and guanylate cyclase activation by nitroglycerin, sodium nitrite, and amyl nitrite

Gruetter, Carl A.; Kadowitz, Philip J.; Ignarro, Louis J.

doi:10.1139/y81-025

Cited by 316 publications

(106 citation statements)

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“…Therefore it is suggested that NO is involved in the CPAinduced relaxation of rat arteries. Further evidence supporting this idea is that the NO pathway inhibitors, such as the NO synthase inhibitor, L-NOARG (Moore et al, 1990), the NO scavenger, haemoglobin (Gruetter et al, 1981) and the soluble guanylate cyclase inhibitor with cyclic GMP-lowering activity, LY83583 (Malta et al, 1988;MUlsch et al, 1988) each suppressed both the CPA-induced relaxation and cyclic GMP formation.…”

Section: Discussionmentioning

confidence: 97%

Relaxation of rat thoracic aorta induced by the Ca²⁺‐ATPase inhibitor, cyclopiazonic acid, possibly through nitric oxide formation

Moritoki

Hisayama

Takeuchi

et al. 1994

British J Pharmacology

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1 The effect of the Ca2+-ATPase inhibitor, cyclopiazonic acid (CPA), was studied on rat thoracic aortic ring preparations. 2 At concentrations above 0.3 JM, CPA induced relaxation in the arteries precontracted with phenylephrine. Removal of the endothelium abolished CPA-induced relaxation.3 The nitric oxide (NO) synthase inhibitor NG-nitro L-arginine (3-300 AM), the free radical scavenger haemoglobin (O.1-33 AM), the soluble guanylate cyclase inhibitor, LY83583 (0.1-10 JAM), each inhibited the endothelium-dependent relaxation to CPA. The potassium channel blocker, glibenclamide (1O AM) and cyclo-oxygenase inhibitor, indomethacin (100 JAM for 60 min and then washed out) did not alter the action of CPA. 4 The calmodulin inhibitors calmidazolium (3-10 IAM) and W-7 (100 AM) also abolished CPA-induced relaxation.5 CPA (10 AM) increased guanosine 3':5'-cyclic monophosphate (cyclic GMP) levels in arteries with an intact endothelium, without affecting adenosine 3':5'-cyclic monophosphate (cyclic AMP) levels. 6 The inhibitors of NO synthesis and actions, the calmodulin inhibitor and removal of the endothelium abolished the CPA-stimulated increase in the levels of cyclic GMP. 7 In Ca2'-free solution, CPA failed to induce relaxation or to stimulate cyclic GMP production.Relaxation to nitroprusside was not affected under these conditions.

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Section: Discussionmentioning

confidence: 97%

Relaxation of rat thoracic aorta induced by the Ca²⁺‐ATPase inhibitor, cyclopiazonic acid, possibly through nitric oxide formation

Moritoki

Hisayama

Takeuchi

et al. 1994

British J Pharmacology

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“…In addition, inability of atropine to attenuate the relaxation by the nerve stimulation (Toda, 1975(Toda, , 1982a excludes the in volvement of a cholinergic mechanism. Relaxations induced by transmural electrical stimulation and nicotine were abolished by methylene blue, a gua nylate cyclase inhibitor (Gruetter et al, 1981). Therefore, the transmitter substance released from the vasodilator nerve may act on smooth muscle and activate guanylate cyclase, thus increasing cy-N. TODA clic GMP levels, and inhibitions of the relaxant re sponse by hemolysate may result from decreased cyclic GMP production.…”

Section: Discussionmentioning

confidence: 99%

Hemolysate Inhibits Cerebral Artery Relaxation

Toda

1988

J Cereb Blood Flow Metab

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Summary: In helical strips of dog middle cerebral arteries partially contracted with prostaglandin (PG) F2a, relax ations induced by angiotensin-II, possibly mediated by PGI2, and those induced by PGH2 were reversed to a contraction or markedly reduced by treatment with he molysate, which, however, attenuated the PGIz-induced relaxation only slightly. The relaxant response of human middle cerebral arterial strips to PGHz was also sup pressed by hemolysate. Dog and monkey middle cerebral arteries responded to transmural electrical stimulation and nicotine with transient relaxations, which were quite susceptible to tetrodotoxin and hexamethonium, respec tively; the relaxations were abolished almost completely by hemolysate and methylene blue. On the other hand, the relaxant response of dog cerebral arteries to a low concentration of K + was not influenced by hemolysate or by methylene blue, but was reversed to a contraction by treatment with ouabain. Relaxations induced by subProlonged cerebral vasospasm after subarach noid hemorrhage evokes severe impairment of local cerebral blood flow, frequently resulting in fatal brain dysfunction. Constituents of erythrocytes and substances produced during the course of hemo lysis of a blood clot appear to play an important role in the genesis of cerebral vasospasm (White, 1983a,b), as injections of autologous blood into ce rebral subarachnoid space provokes angiographic ally verified vasospasm in monkeys, dogs, and rats (Allen and Bahr, 1979; Barry et aI., 1979; Ritchie et aI., 1980), and hemolysate applied in vitro and in situ intensively contracts large cerebral arteries (Osaka, 1977; Ozaki and Mullan, 1979; Toda et aI., 1980). Such an arterial smooth muscle contraction is hypothesized to be associated with vasocon strictor prostaglandins (PGs) liberated from the 46stance-P and nitroglycerin were markedly inhibited by hemolysate; removal of endothelium abolished the relax ation by substance-P, but did not influence the nitroglyc erin-induced relaxation. Hemolysate may interfere with the biosynthesis of PGI2 in the vascular wall, thereby re versing the relaxation induced by angiotensin-II and PGH2 to a contraction. Relaxations induced by electrical and chemical stimulation of vasodilator nerves inner vating cerebral arteries appear to be elicited by a mecha nism dependent on cellular cyclic guanosine monophos phate (GMP), like that underlying the substance-P-in duced and nitroglycerin-induced relaxation. These actions of hemolysate may be involved in the genesis of cerebral vasospasm after subarachnoid hemorrhage. Key Words: Cerebral artery relaxation-Erythrocyte break down products-Prostacyclin-Prostaglandin H2-Va sodilator nerve.

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“…Nitrite has been shown to exhibit vasodilatating activity in vitro at high concentrations [1][2][3][4][5][6][7].…”

Section: Introductionmentioning

confidence: 99%

Magnetic resonance study of the transmembrane nitrite diffusion

et al. 2007

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Nitrite (NO 2 -), being a product of metabolism of both nitric oxide (NO • ) and nitrate (NO 3 -), can accumulate in tissues and regenerate NO • by several mechanisms. The effect of NO 2 -on ischemia/ reperfusion injury was also reported. Nevertheless, the mechanisms of intracellular NO 2 -accumulation are poorly understood. We suggested significant role of nitrite penetration through biological membranes in the form of undissociated nitrous acid (HNO 2 ). This hypothesis has been tested using large unilamellar phosphatidylcholine liposomes and several spectroscopic techniques. HNO 2 transport across the phospholipid bilayer of liposomes facilitates proton transfer resulting in intraliposomal acidification, which was measured using pH-sensitive probes. NO 2 --mediated intraliposomal acidification was confirmed by EPR spectroscopy using membrane-impermeable pHsensitive nitroxide, 2,2,5,5-tetramethyl-1-oxyl-2,5-dihydro-1H-imidazol-3-ium-4-yl)-aminomethanesulfonic acid (pK 5.25), and by 31 P-NMR spectroscopy using inorganic phosphate (pK 6.9). Nitrite accumulates inside liposomes in concentration exceeding its concentration in the bulk solution, when initial transmembrane pH gradient (alkaline inside) is applied. Intraliposomal accumulation of NO 2 -was observed by direct measurement using chemiluminescence technique. Perfusion of isolated rat hearts with buffer containing 4 μM NO 2 -was performed. The nitrite concentrations in the effluent and in the tissue, measured after 1 minute perfusion were close, supporting fast penetration of the nitrite through the tissue. Measurements of the nitrate/nitrate showed that total concentration of NO x in myocardium increased from initial 7.8 μM to 24.7 μM after nitrite perfusion. Physiological significance of passive transmembrane transport of NO 2 -and its coupling with intraliposomal acidification are discussed.

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Methylene blue inhibits coronary arterial relaxation and guanylate cyclase activation by nitroglycerin, sodium nitrite, and amyl nitrite

Cited by 316 publications

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Relaxation of rat thoracic aorta induced by the Ca²⁺‐ATPase inhibitor, cyclopiazonic acid, possibly through nitric oxide formation

Relaxation of rat thoracic aorta induced by the Ca²⁺‐ATPase inhibitor, cyclopiazonic acid, possibly through nitric oxide formation

Hemolysate Inhibits Cerebral Artery Relaxation

Magnetic resonance study of the transmembrane nitrite diffusion

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Methylene blue inhibits coronary arterial relaxation and guanylate cyclase activation by nitroglycerin, sodium nitrite, and amyl nitrite

Cited by 316 publications

References 0 publications

Relaxation of rat thoracic aorta induced by the Ca2+‐ATPase inhibitor, cyclopiazonic acid, possibly through nitric oxide formation

Relaxation of rat thoracic aorta induced by the Ca2+‐ATPase inhibitor, cyclopiazonic acid, possibly through nitric oxide formation

Hemolysate Inhibits Cerebral Artery Relaxation

Magnetic resonance study of the transmembrane nitrite diffusion

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Relaxation of rat thoracic aorta induced by the Ca²⁺‐ATPase inhibitor, cyclopiazonic acid, possibly through nitric oxide formation

Relaxation of rat thoracic aorta induced by the Ca²⁺‐ATPase inhibitor, cyclopiazonic acid, possibly through nitric oxide formation