scholarly journals Stimulatory Effects of Nitric Oxide Donors on Histamine Release in Isolated Rat Gastric Mucosal Cells

2003 ◽  
Vol 26 (7) ◽  
pp. 950-953 ◽  
Author(s):  
Ko Hasebe ◽  
Syunji Horie ◽  
Shingo Yano ◽  
Kazuo Watanabe
Keyword(s):  
Nitric Oxide ◽  
Histamine Release ◽  
Nitric Oxide Donors ◽  
Gastric Mucosal Cells ◽  
Mucosal Cells ◽  
Isolated Rat

scholarly journals Effects of nitric oxide donors on hormone- induced Ca2+ mobilization and cAMP accumulation in isolated rat hepatocytes

1998 ◽  
Vol 76 ◽  
pp. 94
Author(s):  
Shigeru Matsui ◽  
Takahide Nomura ◽  
Masatsugu Ohtsuki ◽  
Masahiro Tazawa ◽  
Chiho Sumi-Ichinose ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Rat Hepatocytes ◽  
Nitric Oxide Donors ◽  
Camp Accumulation ◽  
Isolated Rat Hepatocytes ◽  
Isolated Rat

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.

Nitric oxide generators and cGMP stimulate mucus secretion by rat gastric mucosal cells

1993 ◽  
Vol 265 (3) ◽  
pp. G418-G422 ◽  
Author(s):  
J. F. Brown ◽  
A. C. Keates ◽  
P. J. Hanson ◽  
B. J. Whittle
Keyword(s):  
Nitric Oxide ◽  
Phosphodiesterase Inhibitor ◽  
Mucus Secretion ◽  
Enzyme Linked Immunosorbent Assay ◽  
Gastric Mucus ◽  
Isolated Cells ◽  
Gastric Mucosal Cells ◽  
Trypan Blue Exclusion ◽  
Intracellular Cgmp ◽  
Mucosal Cells

The effect of nitric oxide (NO) donors on the release of mucus from a suspension of isolated gastric cells was investigated by using an enzyme-linked immunosorbent assay for rat gastric mucin. Isosorbide dinitrate (ISDN, 0.1-2 mM) produced a dose-related stimulation of mucus secretion, without affecting the viability of the isolated cells as determined by trypan blue exclusion or acid phosphatase release. In a comparable concentration range to that stimulating mucus release, ISDN elevated the guanosine 3',5'-cyclic monophosphate (cGMP) content of cell suspensions enriched with mucous cells. The nitrosothiol S-nitroso-N-acetylpenicillamine (0.3 mM), which spontaneously liberates NO, likewise stimulated mucus release, and this action was blocked by 10 microM oxyhemoglobin, which scavenges NO. Nitroprusside (1 mM), dibutyryl cGMP (0.01-1 mM), and the cGMP phosphodiesterase inhibitor M & B 22948 (0.1 mM) also increased mucus release. Thus generators of NO stimulate mucus secretion by rat gastric mucosal cells, which may reflect the elevation of intracellular cGMP. These findings, along with the presence of NO synthase in the gastric epithelial cells, suggest an effector role for NO in mediation of gastric mucus release.

scholarly journals Protection by Nitric Oxide Donors of Isolated Rat Hearts Is Associated with Activation of Redox Metabolism and Ferritin Accumulation

PLoS ONE ◽  
2016 ◽  
Vol 11 (7) ◽  
pp. e0159951 ◽  
Author(s):  
Hilbert Grievink ◽  
Galina Zeltcer ◽  
Benjamin Drenger ◽  
Eduard Berenshtein ◽  
Mordechai Chevion
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Donors ◽  
Redox Metabolism ◽  
Rat Hearts ◽  
Isolated Rat
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