The anti‐aggregating properties of vascular endothelium: interactions between prostacyclin and nitric oxide

Abstract

1 The interactions between endothelium-derived nitric oxide (NO) and prostacyclin as inhibitors of platelet aggregation were examined. 2 Porcine aortic endothelial cells treated with indomethacin and stimulated with bradykinin (10-100 nM) released NO in quantities sufficient to account for the inhibition of platelet aggregation attributed to endothelium-derived relaxing factor (EDRF). 3 In the absence of indomethacin, stimulation of the cells with bradykinin (1-3 nM) released small amounts of prostacyclin and EDRF which synergistically inhibited platelet aggregation. 4 EDRF and authentic NO also caused disaggregation of platelets aggregated either with collagen or with U46619. 5 A reciprocal potentiation of both the anti-and the dis-aggregating activity was also observed between low concentrations of prostacyclin and authentic NO or EDRF released from endothelial cells. 6 It is likely that interactions between prostacyclin and NO released by the endothelium play a role in the homeostatic regulation of platelet-vessel wall interactions.

Mechanical stretch reveals different components of endothelial‐mediated vascular tone in rat aortic strips

“…A synergistic antiaggregatory e ect of PGI 2 and NO has been originally described in human platelets: low doses of both compounds inhibit aggregation and induce disaggregation of human platelets, while either PGI 2 or NO alone at the same dose are ine ective (Radomski et al, 1987).…”

Interactive role of nitric oxide and superoxide anion in neutrophil-mediated endothelial cell injury

“…Pober et al [23] have also observed that IFN-␥-induced changes were slower and quantitatively smaller than those observed with interleukin-1␤ and TNF-␣. More recently, NO has been recognized as yet another important molecule that inhibits homotypic platelet aggregation [32], as well as decreases platelet adhesion to EC [24]. To validate the role of NO in PMN-EC adhesion, we added SNAP, a S-nitrosothiol derivative and a stable NO donor [25], to the PMN-EC co-culture.…”

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“…Furthermore, PGI 2 also stimulates the release of EDRF [28]. In addition, NO which accounts for the actions of EDRF [29], potentiates anti-aggregatory properties of PGI 2 ; they both can prevent platelet aggregation together at concentrations which on their own too low to inhibit aggregation [30,31]. NO also inhibits platelet adhesion to the vascular endothelium which contributes to nonthrombogenicity of endothelial cell [32][33][34].…”

“…NO also inhibits platelet adhesion to the vascular endothelium which contributes to nonthrombogenicity of endothelial cell [32][33][34]. The ability of the EE to produce these antithrombotic factors plays an important role in preventing thrombus formation in the cardiac chambers [30,35]. The NO also are involved on atrial fibrillation associated with endothelial dysfunction [36].…”

“…EDNO and PGI 2 may act the synergic way [30] as important anti-thrombotic factor in the atrium. Considering that cultured endothelial cells have shown changes in response to agonists as a result of receptor down-regulation [13,14], the proposed methodology can be more useful due to its easy execution, low cost, good reproducibility and effectiveness in mimicking in vivo conditions.…”