The 10,000 fold effect of retrograde neurotransmission: a new concept for cerebral palsy revival: use of nitric oxide donors (intrathecal sodium nitroprusside and oral tadalafil)

2016 ◽  
Vol 58 ◽  
pp. 33-33
Keyword(s):  
Nitric Oxide ◽  
Cerebral Palsy ◽  
Sodium Nitroprusside ◽  
Nitric Oxide Donors

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

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 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

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

Evidence that Nitric Oxide Inhibits Steroidogenesis in Cultured Rat Granulosa Cells

1997 ◽  
Vol 92 (3) ◽  
pp. 277-284 ◽  
Author(s):  
Shilpa Dave ◽  
David P. Farrance ◽  
Saffron A. Whitehead
Keyword(s):  
Nitric Oxide ◽  
Sodium Nitroprusside ◽  
Granulosa Cells ◽  
Culture Medium ◽  
Nitric Oxide Donors ◽  
Nitrite Accumulation ◽  
High Dose ◽  
Response Curves ◽  
Progesterone Synthesis ◽  
High Concentrations

1. A few studies have shown that nitric oxide may exert cytotoxic and/or steroidogenic effects on cultured ovarian cells but the source of this factor within the ovary remains equivocal. 2. In this study we have investigated the effects of nitric oxide on progesterone secretion, cell viability and cell morphology of cultured rat granulosa/ lutein cells and examined whether granulosa cells are an important source of nitric oxide. 3. Only very low or undetectable levels of nitrites were measured in granulosa/lutein-cell-only cultures, although there was a small but significant increase in nitrite release observed in granulosa/lutein cells obtained from oestrous rats compared with those obtained from proestrous rats. 4. There was a concentration-dependent inhibition of progesterone synthesis in the presence of the nitric oxide donors sodium nitroprusside and S-nitroso-N-acetyl-penicillamine which corresponded with an increased concentration of nitrite accumulation in the culture medium. 5. High concentrations of nitrites were measured in the medium of granulosa/lutein cells co-cultured with peritoneal macrophages and progesterone synthesis was inhibited. This effect of the macrophages was partially reversed by inhibitors of nitric oxide synthesis, aminoguanidine, NG-methyl-l-arginine and NG-l-arginine-methyl-ester, and the reversal of inhibition was inversely proportional to the concentration of nitrites measured in the medium. Dose—response curves for the three drugs on the inhibition of nitrite accumulation in macrophage cultures were obtained. 6. The nitric oxide scavenger c-PTIO [2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide.potassium salt] partially reversed the effects of S-nitroso-N-acetyl-penicillamine and macrophages on progesterone synthesis in granulosa/ lutein cells. 7. With the exception of the high dose of sodium nitroprusside, there was no evidence that any of the drugs reduced cellular viability, as assessed by measurement of cellular dehydrogenases and Trypan Blue exclusion, although high concentrations of nitrite in the culture medium derived either from the nitric oxide donors or macrophages were associated with a loss of morphological luteinization. 8. Based on the available evidence, we suggest that nitric oxide can inhibit steroidogenesis and that in vivo the source of nitric oxide may be from macrophages, which invade the ovary during the periovulatory period, and/or from endothelial cells of ovarian blood vessels.

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.

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