[Expression of inducible nitric oxide synthase in the carotid of rats after endothelial skinning: the effects of platelets and treatment with abciximab].
BACKGROUND
Functional evidence suggests that endothelial denudation stimulates inducible nitric oxide synthase (iNOS) activity in the vascular wall. In vitro studies done in our laboratory have shown that iNOS expression in smooth muscle cells is reduced by endothelial cells. The object of this study was to analyze the iNOS protein expression in the arterial wall after in vivo deendothelialization, and the role of platelet activation abciximab in the expression of this protein.


METHODS
Endothelial denudation was performed in the left carotid artery of Wistar rats. The right carotid artery was used as control.


RESULTS
iNOS protein was only weakly expressed at 6, 24 and 48 hours after endothelial denudation. Since platelet adhesion and aggregation occur early after endothelial damage, we have analyzed the role of activated platelets in iNOS protein expression during the first two days after angioplasty. Early after in vivo endothelial injury, thrombocytopenic rats showed a marked iNOS protein expression. Similar results were obtained by blocking the platelet glycoprotein IIb/IIIa in rats treated with abciximab (Reopro).


CONCLUSIONS
iNOS protein is weakly expressed in the arterial wall after endothelial denudation. Platelets play a crucial role preventing iNOS protein expression early after endothelial damage through a mechanism that depends on GP IIb/IIIa, an effect that can be avoided with glycoprotein IIb/IIIa, blockers, such as abciximab.
González-Fernández
F
F
Laboratorio de Nefrología, Hipertensión e Investigación Cardiovascular, Fundación Jiménez Díaz, Madrid.
Rodríguez-Feo
J A
JA
Farré
J
J
Guerra
J
J
Romero
J
J
Gómez
J
J
Rico
L
L
Ayala
R
R
Marcos
P
P
Sánchez de Miguel
L
L
Casado
S
S
López-Farré
A
A
D000077284:Abciximab; D000818:Animals; D000911:Antibodies, Monoclonal / Q000494:pharmacology*; D001792:Blood Platelets / Q000502:physiology*; D002339:Carotid Arteries / Q000187:drug effects / Q000201:enzymology*; D004730:Endothelium, Vascular / Q000502:physiology*; D004790:Enzyme Induction; D007140:Immunoglobulin Fab Fragments / Q000494:pharmacology*; D066298:In Vitro Techniques; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000201:enzymology*; D019001:Nitric Oxide Synthase / Q000096:biosynthesis*; D052247:Nitric Oxide Synthase Type II; D015539:Platelet Activation; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology*; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors; D051381:Rats; D017208:Rats, Wistar
D000911:Antibodies, Monoclonal; D007140:Immunoglobulin Fab Fragments; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat; D000077284:Abciximab
Expresión de la óxido nítrico sintasa inducible en carótida de rata tras denudación endotelial: efecto de las plaquetas y del tratamiento con abciximab.