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.

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.

The Effect of Inhibition of the Platelet Release Reaction on Platelet Behaviour in vitro and in vivo

2009 ◽  
Vol 9 (1-6) ◽  
pp. 322-332 ◽  
Author(s):  
K.-E. ARFORS ◽  
D. BERGQVIST ◽  
S. BYGDEMAN ◽  
F. N. MCKENZIE ◽  
E. SVENSJÖ
Keyword(s):  
Release Reaction ◽  
Platelet Release

Nitric oxide as a putative nonadrenergic noncholinergic inhibitory transmitter in the canine pylorus in vivo

1992 ◽  
Vol 262 (4) ◽  
pp. G695-G702 ◽  
Author(s):  
H. D. Allescher ◽  
G. Tougas ◽  
P. Vergara ◽  
S. Lu ◽  
E. E. Daniel
Keyword(s):  
Nitric Oxide ◽  
Sodium Nitroprusside ◽  
Vagal Stimulation ◽  
Inhibitory Effect ◽  
Field Stimulation ◽  
Neural Inhibition ◽  
Anesthetized Dogs ◽  
Inhibitory Transmitter

Antropyloroduodenal motility was recorded in seven anesthetized dogs to assess the role of nitric oxide and L-arginine metabolites in nonadrenergic noncholinergic (NANC) mediation of pyloric relaxation. Pyloric activity induced by duodenal field stimulation was inhibited by antral field stimulation and electrical vagal stimulation. Intra-arterial NG-L-arginine-methyl-ester (L-NAME) reduced the inhibition from antral or vagal stimulation (P less than 0.05). Intravenous infusion of L-NAME also blocked the inhibitory effect of vagal and antral stimulation but left the tetrodotoxin-insensitive action of intra-arterial vasoactive intestinal peptide (VIP) and sodium nitroprusside unchanged. L-Arginine reversed the effect of L-NAME whereas D-arginine did not. L-NAME enhanced pyloric contractions to intra-arterial acetylcholine. The NANC inhibition of the substance P-stimulated pyloric response in vitro was blocked by L-NAME and reversed by addition of L-arginine. Sodium nitroprusside was effective as a relaxant in vitro but VIP was not. These data suggest that metabolites of L-arginine mediate neural inhibition of canine pyloric motor activity.

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

The Potentiation of Platelet Aggregation and Adhesion by Heparin in Vitro and in Vivo

1973 ◽  
Vol 45 (4) ◽  
pp. 485-494 ◽  
Author(s):  
C. Thomson ◽  
C. D. Forbes ◽  
C. R. M. Prentice
Keyword(s):  
Platelet Aggregation ◽  
Intravenous Injection ◽  
Whole Blood ◽  
Platelet Rich Plasma ◽  
Test Cell ◽  
Release Reaction ◽  
Platelet Release ◽  
Increase Platelet Aggregation

1. Heparin has been shown to increase platelet aggregation by ADP and adrenaline and to enhance the platelet release reaction when tested in citrated platelet-rich plasma (P.R.P.). This activity is present when heparin is added to P.R.P. or when P.R.P. is prepared after intravenous injection of heparin, and when heparin is added to non-anticoagulated native P.R.P. 2. Retention of platelets by cellophane membranes within a specially designed test-cell was significantly increased when heparin was added to citrated whole blood. 3. Though aspirin blocks the release reaction with and without heparin, it does not prevent the potentiation of initial ADP or first wave adrenaline aggregation caused by heparin.

Correlation of In Vitro and In Vivo Kinetics of Nitric Oxide Donors in Ocular Tissues

2009 ◽  
Vol 25 (2) ◽  
pp. 105-112 ◽  
Author(s):  
Samantha Carreiro ◽  
Scott Anderson ◽  
Hovhannes J. Gukasyan ◽  
Achim Krauss ◽  
Ganesh Prasanna
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Donors ◽  
Ocular Tissues ◽  
In Vivo Kinetics ◽  
Kinetics Of

scholarly journals Pyrogen–prostaglandin coupling in the pathogenesis of fever: evidence against a role for nitric oxide

1995 ◽  
Vol 73 (10) ◽  
pp. 1466-1474 ◽  
Author(s):  
Jane Redford ◽  
Isis Bishai ◽  
Flavio Coceani
Keyword(s):  
Nitric Oxide ◽  
Brain Tissue ◽  
Cyclic Gmp ◽  
Interleukin 1 ◽  
Prostaglandin E ◽  
Signal Transducer ◽  
Cerebral Tissue ◽  
Cerebral Microvessels

There is much debate on the mechanism by which blood-borne pyrogens trigger prostaglandin E2 (PGE2) synthesis in brain and fever. This investigation was undertaken to determine whether nitric oxide qualifies as a signal transducer for pyrogens at the interface between blood and brain. Experiments were carried out in vitro and in vivo using, respectively, preparations of cerebral tissue and microvessels from the rat, and the conscious, chronically instrumented cat. In vitro preparations produced PGE2 and its production increased during a 30-min treatment with interleukin 1 (brain tissue) or endotoxin (microvessels). In addition, both pyrogens increased cyclic GMP levels in cerebral microvessels. In both brain tissue and microvessels, NG-nitro-L-arginine had no effect on basal PGE2 release, while it curtailed the pyrogen-stimulated release. The same treatment reduced the cyclic GMP accumulation brought about by pyrogens in the microvessels. Conversely, in the conscious cat, inhibitors of nitric oxide synthesis (NG-monomethyl-L-argimne, NG-nitro-L-arginine) had no effect on fever and the concomitant elevation of PGE2 in cerebrospinal fluid, regardless of the pyrogen used (endotoxin, interleukin 1) and the route of administration (intravenous, intracerebroventricular). We conclude that nitric oxide may serve as a pyrogen mediator in brain. This mediator function, however, is seemingly not important in the development of fever.Key words: pyrogen, fever mechanism, nitric oxide, prostaglandin E2, blood–brain barrier.

scholarly journals Pendrin protein abundance in the kidney is regulated by nitric oxide and cAMP

2012 ◽  
Vol 303 (6) ◽  
pp. F812-F820 ◽  
Author(s):  
Monika Thumova ◽  
Vladimir Pech ◽  
Otto Froehlich ◽  
Diana Agazatian ◽  
Xiaonan Wang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Pressor Response ◽  
Fluorescent Microscopy ◽  
Phosphodiesterase Inhibitor ◽  
Protein Abundance ◽  
No Donor ◽  
Camp Content

Pendrin is a Cl−/HCO3− exchanger, expressed in the apical regions of some intercalated cell subtypes, and is critical in the pressor response to angiotensin II. Since angiotensin type 1 receptor inhibitors reduce renal pendrin protein abundance in mice in vivo through a mechanism that is dependent on nitric oxide (NO), we asked if NO modulates renal pendrin expression in vitro and explored the mechanism by which it occurs. Thus we quantified pendrin protein abundance by confocal fluorescent microscopy in cultured mouse cortical collecting ducts (CCDs) and connecting tubules (CNTs). After overnight culture, CCDs maintain their tubular structure and maintain a solute gradient when perfused in vitro. Pendrin protein abundance increased 67% in CNT and 53% in CCD when NO synthase was inhibited ( NG-nitro-l-arginine methyl ester, 100 μM), while NO donor (DETA NONOate, 200 μM) application reduced pendrin protein by ∼33% in the CCD and CNT. When CNTs were cultured in the presence of the guanylyl cyclase inhibitor 1H-[1,2,4] oxadiazolo[4,3-a]quinoxalin-1-one (10 μM), NO donors did not alter pendrin abundance. Conversely, pendrin protein abundance rose when cAMP content was increased by the application of an adenylyl cyclase agonist (forskolin, 10 μM), a cAMP analog (8-bromo-cAMP, 1 mM), or a phosphodiesterase inhibitor (BAY60-7550, 50 μM). Since NO reduces cellular cAMP in the CNT, we asked if NO reduces pendrin abundance by reducing cAMP. With blockade of cGMP-stimulated phosphodiesterase II, NO did not alter pendrin protein abundance. We conclude that NO acts through cAMP to reduce pendrin total protein abundance by enhancing cAMP degradation.

scholarly journals Role of cyclic GMP on inhibition by nitric oxide donors of human eosinophil chemotaxis in vitro

2004 ◽  
Vol 141 (4) ◽  
pp. 653-660 ◽  
Author(s):  
Sara M Thomazzi ◽  
Juliana Moreira ◽  
Sisi Marcondes ◽  
Gilberto De Nucci ◽  
Edson Antunes
Keyword(s):  
Nitric Oxide ◽  
Cyclic Gmp ◽  
Nitric Oxide Donors ◽  
Human Eosinophil ◽  
Eosinophil Chemotaxis
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