European Journal of Pharmacology: Molecular Pharmacology
Regular paperEffects of nitric oxide-containing compounds on increases in cytosolic ionized Ca2+ and on aggregation of human platelets☆
References (35)
- et al.
Properties of a novel nitric oxide-stimulated ADP-ribosyltransferase
Arch. Biochem. Biophys.
(1990) - et al.
Different calcium pools in human platelets and their role in thromboxane A2 formation
J. Biol. Chem.
(1991) - et al.
Direct comparison of the effects of nitroprusside, SIN-1, and various nitrates on platelet aggregation and soluble guanylate cyclase activity
Thromb. Res.
(1988) - et al.
A new generation of Ca2+ indicators with greatly improved fluorescence properties
J. Biol. Chem.
(1985) - et al.
Measurement of platelet cytoplasmic ionized calcium concentration with aequorin and fluorescent indicators
- et al.
Inhibitory action of guanosine 3′,5′-monophosphate on thrombin-induced calcium mobilization in human platelets
Thromb. Res.
(1984) - et al.
Regulation of platelet cytosolic free calcium by cyclic nucleotides and protein kinase C
FEBS Lett.
(1985) - et al.
Evidence for the inhibitory role of guanosine 3′,5′-monophosphate in ADP-induced human platelet aggregation in the presence of nitric oxide and related vasodilators
Blood
(1981) - et al.
Inhibitory action of cyclic GMP on secretion, polyphosphoinositide hydrolysis and calcium mobilization in thrombin-stimulated human platelets
Biochem. Biophys. Res. Commun.
(1986) - et al.
Inositol 1,4,5-trisphosphate releases Ca2+ from a Ca2+- transporting membrane vesicle fraction derived from human platelets
J. Biol. Chem.
(1985)
Effects of a stimulant of guanylate cyclase, SIN 1, on calcium movements and phospholipase C activation in thrombin-stimulated human platelets
Biochem. Pharmacol.
Separation of human platelets from plasma proteins including factor VIIIvwf by a combined albumin gradient-gel filtration method using HEPES buffer
Thromb. Res.
Endothelium-derived relaxing factor is a nitrosyl iron complex with thiol ligands
FEBS Lett.
Chemical and kinetic study on stabilities of 3-morpholino-sydnonimine and its N-ethoxycarbonyl derivate
Chem. Pharm. Bull.
Effects of sodium nitroprusside and other smooth muscle relaxants on cyclic GMP formation in smooth muscle and platelets
Adv. Cyclic Nucleotide Res.
Regulation of cyclic GMP formation by soluble guanylate cyclase: stimulation by NO-containing compounds
Adv. Cyclic Nucleotide Protein Phosphorylation Res.
Oxygen and oxydation promote the release of nitric oxide from sydnonimines
J. Cardiovasc. Pharmacol.
Cited by (55)
Inhaled nitric oxide improves post-cardiac arrest outcomes via guanylate cyclase-1 in bone marrow-derived cells
2022, Nitric Oxide - Biology and ChemistryCitation Excerpt :We observed that CA/CPR increased platelet P-selectin expression, TXA2 secretion, and hypercoagulability, suggesting platelet activation in post-CA mice. NO/GC/cGMP signaling inhibits platelet aggregation [18,32–36], secretion [70], adhesion [71], and binding of fibrinogen to its integrin receptor, GpIIb/IIIa, on the platelet membrane [72–74]. Along these lines, we observed that iNO inhibited the platelet activation and secretion of TXA2 and attenuated hypercoagulability and cerebral microvascular occlusion after CA/CPR.
Protein kinase A mediates inhibition of the thrombin-induced platelet shape change by nitric oxide
2004, BloodCitation Excerpt :Regulation of platelet activation is an important physiologic function of the vascular endothelium including release of nitric oxide (NO),13 a potent inhibitor of platelet aggregation, secretion, adhesion, and binding of fibrinogen to integrin glycoprotein IIbIIIa (GpIIbIIIa).14-17 Conflicting results have, however, been reported about the effect of NO on shape change.18-21 The inhibitory effects of NO on platelet activation have been considered to be due to activation of the soluble guanylyl cyclase causing production of cyclic guanosine monophosphate (cGMP) and subsequent activation of cGMP-dependent protein kinase G (PKG).22
Differential expression of functional guanylyl cyclases in melanocytes: Absence of nitric-oxide-sensitive isoform in metastatic cells
2001, Journal of Investigative DermatologyCitation Excerpt :For testing the activation of sGC, melanocytes were treated for 5 min with SIN-1 (0.01–1 mM) (Feelisch et al. 1989;Ivanova et al. 1993). Denitrosylated solutions of SIN-1 (which contain the inactive byproducts) as controls were obtained as described elsewhere (Ivanova et al. 1997). For activation of GC-A, GC-B, and GC-C the melanocytes were incubated for 15 min with human α-ANP1-28, BNP32, CNP22, guanylin (Peninsula Lab., St. Helens, U.K.), and STa toxin (Sigma, St. Louis, MO) in the range of 0.001–1 μM.
- ☆
Preliminary results of this study have been reported at the ‘Wintertagung der Deutschen Gessellschaft für Pharmakologie’ (Ivanova et al., 1991).