Platelet inhibition by endothelium-derived relaxing factor from the rabbit perfused aorta
| Autor: | Arnold G. Herman, Hidde Bult, Rita M. Van den Bossche, Hermine R.L. Fret |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 1988 |
| Předmět: |
Endothelium
Platelet Aggregation Indomethacin Prostacyclin Aorta Thoracic Pharmacology In Vitro Techniques Nitric Oxide Nitric oxide chemistry.chemical_compound Biological Factors medicine.artery medicine Thoracic aorta Animals Platelet Aorta Endothelium-derived relaxing factor Anatomy Epoprostenol Acetylcholine Perfusion medicine.anatomical_structure chemistry cardiovascular system lipids (amino acids peptides and proteins) Endothelium Vascular Rabbits medicine.symptom Vasoconstriction medicine.drug circulatory and respiratory physiology Research Article |
| Popis: | 1. The platelet inhibiting activity of endothelium-derived relaxing factor (EDRF) released by the perfused thoracic aorta of the rabbit was investigated. 2. The aortic effluent superfused a ring of the abdominal aorta without endothelium in order to bioassay EDRF. Aliquots of effluent were collected on rabbit washed platelets and aggregation induced by U-46619 was measured after 1 min. Prostacyclin (PGI2) was monitored by radioimmunoassay of 6-oxo-prostaglandin F1 alpha. 3. Acetylcholine (ACh) caused a dose-dependent secretion of EDRF, PGI2 and anti-aggregating activity. Plasma and methylene blue suppressed the platelet inhibition by the effluent. 4. The PGI2 content of the effluent was not sufficient to account for all the anti-aggregating activity. However, the platelet inhibition disappeared when PGI2 formation was blocked with indomethacin. 5. Compression of the thoracic aorta increased the EDRF content in the effluent. A transient secretion of anti-aggregating activity was then observed in aortic effluent in the absence of PGI2. This activity coincided with the presumed EDRF peak in the effluent. 6. Superoxide dismutase enhanced the ACh-induced EDRF content and revealed secretion of an anti-aggregating substance when PGI2 formation was blocked. Pretreatment of the platelets with subthreshold concentrations of PGI2, or the cyclic GMP phosphodiesterase inhibitor RX-RE 56, also revealed the release of a labile platelet inhibitor in response to ACh. 7. The results indicate that EDRF released by fresh aortic endothelium may suppress platelet aggregation, particularly when PGI2 is present. |
| Databáze: | OpenAIRE |
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