Interaction of antiplatelet drugs in vitro: Aspirin, iloprost, and the nitric oxide donors SIN-1 and sodium nitroprusside

1995 ◽  
Vol 9 (4) ◽  
pp. 619-629 ◽  
Author(s):  
Emil V. Negrescu ◽  
Bernd Gr�nberg ◽  
Michael A. A. Kratzer ◽  
Reinhard Lorenz ◽  
Wolfgang Siess
Keyword(s):  
Nitric Oxide ◽  
Sodium Nitroprusside ◽  
Antiplatelet Drugs ◽  
Nitric Oxide Donors

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

Effects of Nitric Oxide Donors in Vitro on the Arachidonic Acid-Induced Platelet Release Reaction and Platelet Cyclic GMP Concentration in Pre-Eclampsia

1994 ◽  
Vol 86 (2) ◽  
pp. 195-202 ◽  
Author(s):  
E. Hardy ◽  
P. C. Rubin ◽  
E. H. Horn
Keyword(s):  
Nitric Oxide ◽  
Sodium Nitroprusside ◽  
Cyclic Gmp ◽  
Phosphodiesterase Inhibitor ◽  
Nitric Oxide Donors ◽  
Release Reaction ◽  
Healthy Pregnancy ◽  
Platelet Release

1. Platelet activation in vivo occurs in healthy pregnancy and is more pronounced in pre-eclampsia. 2. This study has investigated: (i) the inhibitory potency of the nitric oxide donors 3-morpholinosydnonimine and sodium nitroprusside, on the platelet release reaction in vitro in non-pregnant, healthy pregnant and pre-eclamptic women; (ii) the concentration of cyclic GMP during incubation of washed platelets with sodium nitroprusside in a separate group of non-pregnant, healthy pregnant and pre-eclamptic women. 3. The half-maximal inhibitory concentration of sodium nitroprusside, in the presence of a phosphodiesterase inhibitor, for inhibition of the platelet release reaction was lower in the pre-eclamptic subjects than in the non-pregnant subjects (P < 0.05). 4. Several of the pre-eclamptic women were studied again postnatally. The half-maximal inhibitory concentrations of sodium nitroprusside and 3-morpholinosydnonimine were higher in the postnatal than in the antenatal sample (P < 0.02). 5. Peak platelet cyclic GMP responses to sodium nitroprusside were significantly higher in the pre-eclamptic women than in the healthy pregnant and non-pregnant women. 6. These results suggest that platelets are more sensitive to the inhibitory effects of nitric oxide donors in pre-eclampsia.

Effects of sodium nitroprusside(a donor of nitric oxide) on development of porcine preantral follicle cultured in vitro

2011 ◽  
Vol 37 (1) ◽  
pp. 55-59
Author(s):  
Qing QUAN ◽  
Yong TAO ◽  
Xiao-rong ZHANG ◽  
Gui-dong YAO ◽  
Jin-ju WANG
Keyword(s):  
Nitric Oxide ◽  
Sodium Nitroprusside ◽  
Preantral Follicle

scholarly journals Nitric Oxide Donors Suppress Chemokine Production by Keratinocytes in Vitro and in Vivo

2002 ◽  
Vol 161 (4) ◽  
pp. 1409-1418 ◽  
Author(s):  
Maria Laura Giustizieri ◽  
Cristina Albanesi ◽  
Claudia Scarponi ◽  
Ornella De Pità ◽  
Giampiero Girolomoni
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Donors ◽  
Chemokine Production

Characterization of acute reversible systemic hypertension in a model of heme protein-induced renal injury

1999 ◽  
Vol 277 (1) ◽  
pp. F58-F65 ◽  
Author(s):  
David H. Warden ◽  
Anthony J. Croatt ◽  
Zvonimir S. Katusic ◽  
Karl A. Nath
Keyword(s):  
Nitric Oxide ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sodium Nitroprusside ◽  
Vessel Wall ◽  
Heme Proteins ◽  
Blood Vessel Wall ◽  
Vasodilatory Response

In the glycerol model of renal injury we describe an acute rise in systemic arterial pressure which is attended by a reduced vasodilatory response to acetylcholine in vivo; vasodilatory responses to verapamil, however, were not impaired. Neither arginine nor sodium nitroprusside diminished this rise in blood pressure; N ω-nitro-l-arginine methyl ester (l-NAME) elevated basal mean arterial pressure and markedly blunted the rise in mean arterial pressure following the administration of glycerol. Aortic rings from the glycerol-treated rat demonstrate an impaired vasodilatory response to acetylcholine, an effect not repaired by arginine; the vasodilatory responses to nitric oxide donors, sodium nitroprusside and SIN-1, were also impaired; 8-bromo-cGMP, at higher doses, evinced a vasodilatory response comparable to that observed in the control rings. This pattern of responses was not a nonspecific effect of aortic injury, since aortic rings treated with mercuric chloride, a potent oxidant, displayed an impaired vasodilatory response to acetylcholine but not to sodium nitroprusside. We conclude that in the glycerol model of heme protein-induced tissue injury, there is an acute elevation in mean arterial pressure attended by impaired endothelium-dependent vasodilatation in vitro and in vivo. We suggest that the acute scavenging of nitric oxide by heme proteins depletes the blood vessel wall of its endogenous vasodilator and permeation of heme proteins into the blood vessel wall may contribute to such sustained effects as observed in vitro.

Comparison of the mechanisms underlying the relaxation induced by two nitric oxide donors: Sodium nitroprusside and a new ruthenium complex

2007 ◽  
Vol 46 (3) ◽  
pp. 215-222 ◽  
Author(s):  
Daniella Bonaventura ◽  
Renata Galvão de Lima ◽  
Juliana A. Vercesi ◽  
Roberto Santana da Silva ◽  
Lusiane M. Bendhack
Keyword(s):  
Nitric Oxide ◽  
Sodium Nitroprusside ◽  
Ruthenium Complex ◽  
Nitric Oxide Donors

Effect of nitric oxide donors on NADPH oxidase signaling pathway in human neutrophils in vitro

Immunobiology ◽  
2009 ◽  
Vol 214 (8) ◽  
pp. 692-702 ◽  
Author(s):  
Magdalena Klink ◽  
Katarzyna Jastrzembska ◽  
Katarzyna Bednarska ◽  
Małgorzata Banasik ◽  
Zofia Sulowska
Keyword(s):  
Nitric Oxide ◽  
Nadph Oxidase ◽  
Signaling Pathway ◽  
Human Neutrophils ◽  
Nitric Oxide Donors

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.

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