scholarly journals NO to cancer: The complex and multifaceted role of nitric oxide and the epigenetic nitric oxide donor, RRx-001

Redox Biology ◽  
2015 ◽  
Vol 6 ◽  
pp. 1-8 ◽  
Author(s):  
Jan Scicinski ◽  
Bryan Oronsky ◽  
Shoucheng Ning ◽  
Susan Knox ◽  
Donna Peehl ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Donor

Nitric oxide attenuates endothelin-1-induced vasoconstriction in canine stomach

1996 ◽  
Vol 271 (1) ◽  
pp. G27-G35
Author(s):  
J. G. Wood ◽  
Q. Zhang ◽  
Z. Y. Yan ◽  
L. Y. Cheung
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Ischemia Reperfusion ◽  
Nitric Oxide Donor ◽  
Question Mark ◽  
Endothelin 1 ◽  
Vasoconstrictor Response ◽  
Anesthetized Dogs ◽  
Spermine Nonoate

We previously observed that endothelin-1 (ET-1)-induced gastric vasoconstriction is enhanced after ischemia-reperfusion. The purpose of our present study was to examine the role of nitric oxide in regulating ET-1-induced vasoconstriction under normal conditions and after ischemia-reperfusion. Using a mechanically perfused stomach segment from chloralose-anesthetized dogs, we examined 1) responses to NG-nitro-L-arginine methyl ester (L-NAME) alone and in combination with L-arginine, 2) whether L-NAME affects ET-1-induced vasoconstriction under normal conditions and after ischemia-reperfusion, and 3) if spermine NONOate inverted question mark1,3-propanediamine-N-[4-1-(3-aminopropyl)-2-hydroxy-2-nitrosohydrazi no] butyl; a nitric oxide donor inverted question mark attenuates the augmented response to ET-1 after ischemia-reperfusion. Our results show that 1) L-NAME significantly increased baseline vascular resistance and this response was reduced by L-arginine, 2) ET-1-induced vasoconstriction was enhanced by L-NAME, and 3) administration of spermine NONOate during reperfusion largely attenuated the vasoconstrictor response to ET-1 after ischemia-reperfusion. Our findings are consistent with the hypothesis that nitric oxide modulates responses to ET-1 under normal conditions, and loss of this vasodilator after ischemia-reperfusion results in an augmented response to ET-1.

Role of the nitric oxide donor sodium nitroprusside in the antidepressant effect of ketamine in mice

2015 ◽  
Vol 25 (10) ◽  
pp. 1848-1852 ◽  
Author(s):  
Miriam A. Vogt ◽  
Anne S. Vogel ◽  
Natascha Pfeiffer ◽  
Peter Gass ◽  
Dragos Inta
Keyword(s):  
Nitric Oxide ◽  
Sodium Nitroprusside ◽  
Nitric Oxide Donor ◽  
Antidepressant Effect

Role of K+Channels in Augmented Relaxations to Sodium Nitroprusside Induced by Mexiletine in Rat Aortas

2000 ◽  
Vol 92 (3) ◽  
pp. 813-820 ◽  
Author(s):  
Hiroyuki Kinoshita ◽  
Toshizo Ishikawa ◽  
Yoshio Hatano
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Sodium Nitroprusside ◽  
Guanylate Cyclase ◽  
Nitric Oxide Donor ◽  
Nitric Oxide Donors ◽  
K Channels ◽  
Vasodilator Effect ◽  
Isolated Rat

Background A class Ib antiarrhythmic drug, mexiletine, augments relaxations produced by adenosine triphosphate (ATP) sensitive K+ channel openers in isolated rat aortas, suggesting that it produces changes in the vasodilation mediated by ATP-sensitive K+ channels. Nitric oxide can induce its vasodilator effect via K+ channels, including ATP-sensitive K+ channels, in smooth muscle cells. Effects of mexiletine on arterial relaxations to nitric oxide donors, have not been studied. Therefore, the current study in isolated rat aortas was designed to (1) evaluate whether mexiletine augments relaxation in response to nitric oxide donors, including sodium nitroprusside, and (2) determine the role of K+ channels in mediating effects of mexiletine on such nitric oxide-mediated relaxation. Methods Rings of rat aortas without endothelia were suspended for isometric force recording. Concentration-response curves of sodium nitroprusside (10(-10) to 10(-5) M) and 1-hydroxy-2-oxo-3-(N-methyl-3-aminopropyl)-3-methyl-1-triazene (NOC-7; 10(-9) to 10(-5) M) were obtained in the absence and in the presence of mexiletine, in combination with a soluble guanylate cyclase inhibitor, 1H-[1,2,4]oxadiazolo [4,3,-a]quinoxaline-1-one (ODQ), or inhibitors for ATP-sensitive K+ channels (glibenclamide), inward rectifier K+ channels (BaCl2), delayed rectifier K+ channels (4-aminopyridine), large conductance Ca2+-dependent K+ channels (iberiotoxin), or small conductance Ca2+-dependent K+ channels (apamin). Results Mexiletine (10(-5) or 3 x 10(-5) M) augmented relaxations to sodium nitroprusside and NOC-7. In arteries treated with glibenclamide (10(-5) M), mexiletine (3 x 10(-5) M) did not affect relaxations to nitric oxide donors, whereas mexiletine augmented relaxations to sodium nitroprusside despite the presence of BaCl2 (10(-5) M), 4-aminopyridine (10(-3) M), iberiotoxin (5 x 10(-8) M) and apamin (5 x 10(-8) M). Relaxations to sodium nitroprusside were abolished by ODQ (5 x 10(-6) M), whereas these relaxations were augmented by mexiletine (3 x 10(-5) M) in arteries treated with ODQ (5 x 10(-6) M). Conclusions These results suggest that ATP-sensitive K+ channels in vascular smooth muscle, contribute to the augmented vasodilator effect of a nitric oxide donor, sodium nitroprusside induced by mexiletine, and that the vasodilator effect is produced, at least in part, via the guanylate cyclase-independent mechanism.

scholarly journals Role of the nitric oxide donor linsidomine chlorhydrate (SIN-1) in the diagnosis and treatment of erectile dysfunction

Urology ◽  
1994 ◽  
Vol 44 (4) ◽  
pp. 553-556 ◽  
Author(s):  
Michael C. Truss ◽  
Armin J. Becker ◽  
Mohamad H. Djamilian ◽  
Christian G. Stiff ◽  
Udo Jonas
Keyword(s):  
Nitric Oxide ◽  
Erectile Dysfunction ◽  
Diagnosis And Treatment ◽  
Nitric Oxide Donor

Endothelial L-arginine pathway and relaxations to vasopressin in canine basilar artery

1993 ◽  
Vol 264 (2) ◽  
pp. H413-H418 ◽  
Author(s):  
F. Cosentino ◽  
J. C. Sill ◽  
Z. S. Katusic
Keyword(s):  
Nitric Oxide ◽  
Basilar Artery ◽  
Isometric Tension ◽  
Nitric Oxide Donor ◽  
Basal Tone ◽  
Basilar Arteries ◽  
Canine Basilar Artery ◽  
Subsequent Activation ◽  
Oxide Synthase

Experiments were designed to determine the role of the L-arginine pathway in endothelium-dependent relaxations to vasopressin. The effects of L-arginine analogues NG-nitro-L-arginine (L-NNA), NG-nitro-L-arginine methyl ester (L-NAME), and NG-monomethyl-L-arginine (L-NMMA) on basal and vasopressin-induced activity of nitric oxide synthase were studied in isolated canine basilar arteries. Rings with and without endothelium were suspended for isometric tension recording in Krebs-Ringer bicarbonate solution bubbled with 94% O2-6% CO2 (37 degrees C, pH 7.4). Radioimmunoassay was used to determine the level of guanosine 3',5'-cyclic monophosphate (cGMP). All experiments were performed in the presence of indomethacin, a cyclooxygenase inhibitor. L-NAME and L-NMMA caused endothelium-dependent contractions and inhibited basal production of cGMP. In contrast, L-NNA did not affect basal tone or basal production of cGMP. L-Arginine analogues inhibited relaxations to vasopressin but did not affect relaxations to a nitric oxide donor, molsidomine (SIN-1). The effects of L-NNA, L-NAME, and L-NMMA were reversed in the presence of L-arginine. The relaxations to vasopressin were associated with an increase of cGMP levels in the arterial wall. This effect of vasopressin was inhibited in the presence of L-NNA. These studies suggest that the relaxations to vasopressin are mediated by activation of the endothelial L-arginine pathway, leading to increased production of nitric oxide, with subsequent activation of guanylate cyclase in smooth muscle cells. In canine basilar artery, L-NAME and L-NMMA are nonselective inhibitors of both basal and stimulated production of nitric oxide, whereas L-NNA selectively inhibits vasopressin-induced activation of the L-arginine pathway.

Atherogenic role of lysophosphatidylcholine in low-density lipoprotein modified by phospholipase A2 and in diabetic patients: Protection by nitric oxide donor

Metabolism ◽  
2003 ◽  
Vol 52 (3) ◽  
pp. 308-314 ◽  
Author(s):  
Kazuo Sonoki ◽  
Masanori Iwase ◽  
Kenzo Iino ◽  
Kojiro Ichikawa ◽  
Shigehiro Ohdo ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Phospholipase A2 ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Nitric Oxide Donor ◽  
Diabetic Patients ◽  
Low Density

The role of pre-ischaemic application of the nitric oxide donor spermine/nitric oxide complex in enhancing flap survival in a rat model

2002 ◽  
Vol 55 (5) ◽  
pp. 430-433 ◽  
Author(s):  
Markus V. Küntscher ◽  
Sebastian Juran ◽  
Henrik Menke ◽  
Detlev Erdmann ◽  
Günter Germann ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Rat Model ◽  
Nitric Oxide Donor ◽  
Flap Survival

scholarly journals Nitric oxide inhibits isoproterenol-stimulated adipocyte lipolysis through oxidative inactivation of the β-agonist

2000 ◽  
Vol 351 (2) ◽  
pp. 485-493 ◽  
Author(s):  
Peter KLATT ◽  
Judith CACHO ◽  
M. Dolores CRESPO ◽  
Emilio HERRERA ◽  
Pilar RAMOS
Keyword(s):  
Nitric Oxide ◽  
Adipose Tissue ◽  
Lipolytic Activity ◽  
Effective Concentration ◽  
Nitric Oxide Donor ◽  
Oxidation Reactions ◽  
Oxidative Inactivation ◽  
Pre Treatment

Nitric oxide has been implicated in the inhibition of catecholamine-stimulated lipolysis in adipose tissue by as yet unknown mechanisms. In the present study, it is shown that the nitric oxide donor, 2,2-diethyl-1-nitroso-oxyhydrazine, antagonized isoproterenol (isoprenaline)-induced lipolysis in rat adipocytes, freshly isolated from white adipose tissue, by decreasing the potency of the β-agonist without affecting its efficacy. These data suggest that nitric oxide did not act downstream of the β-adrenoceptor but reduced the effective concentration of isoproterenol. In support of the latter hypothesis, we found that pre-treatment of isoproterenol with nitric oxide abolished the lipolytic activity of the catecholamine. Spectroscopic data and HPLC analysis confirmed that the nitric oxide-mediated inactivation of isoproterenol was in fact because of the modification of the catecholamine through a sequence of oxidation reactions, which apparently involved the generation of an aminochrome. Similarly, aminochrome was found to be the primary product of isoproterenol oxidation by 3-morpholinosydnonimine and peroxynitrite. Finally, it was shown that nitric oxide released from cytokine-stimulated adipocytes attenuated the lipolytic effect of isoproterenol by inactivating the catecholamine. In contrast with very recent findings, which suggest that nitric oxide impairs the β-adrenergic action of isoproterenol through intracellular mechanisms and not through a chemical reaction between NO and the catecholamine, we showed that nitric oxide was able to attenuate the pharmacological activity of isoproterenol in vitro as well as in a nitric oxide-generating cellular system through oxidation of the β-agonist. These findings should be taken into account in both the design and interpretation of studies used to investigate the role of nitric oxide as a modulator of isoproterenol-stimulated signal transduction pathways.

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