Ibuprofen or ozagrel increases NO release and l-nitro arginine induces TXA2 release from cultured porcine basilar arterial endothelial cells

Orchidectomy increases the formation of non-endothelial thromboxane A2 and modulates its role in the electrical field stimulation-induced response in rat mesenteric artery

“…Therefore, we studied the effect of the TXA 2 synthesis inhibitor furegrelate, on the release and function of neuronal NO, as well as the dependence on endogenous male sex hormones. We found that in arteries from control rats, furegrelate increased the neuronal NO release, which is in line with reports describing an inhibitory effect of TXA 2 on inducible (Yamada et al 2003) and endothelial (Miyamoto et al 2007) NO release. The vasodilator response induced by the NO donor, SNP, was also increased by furegrelate, showing that endogenous TXA 2 negatively modulates both the release and the vasodilator effect of neuronal NO.…”

“…Moreover, regarding the specific action of TXA 2 on the NO system, a decrease in inducible (Yamada et al 2003) as well as endothelial (Miyamoto et al 2007) NO release has been reported. However, details about the action of TXA 2 on neuronal NO release in vascular tissue remain unknown.…”

Androgens and Vascular Function

“…prostaglandin (PG) I 2 increased neuronal NO release (Ferrer et al, 2004) and taking into account that in our experimental conditions the main neurotransmitters involved in that response elicited by EFS were NO and NA, we investigated the regulation of the NA and NO release and function by TXA 2 . We observed that in arteries from control rats, the TXA 2 synthesis inhibition, with furegrelate, increased the neuronal NO release, which was in line with reports describing an inhibitory effect of TXA 2 on inducible (Yamada et al, 2003) and endothelial (Miyamoto et al, 2007) NO release. The vasodilator response induced by the NO donor, sodium nitroprusside was also increased by furegrelate.…”

Thromboxane A2-induced Bi-directional Regulation of Cerebral Arterial Tone

“…TXA 2 , secreted from platelets (75) and from cerebrovascular endothelial cells (76), positively modulates vasoconstriction, whereas endothelium-derived NO and prostaglandin I 2 (77) positively modulate vasorelaxation. Luminal perfusion of TXA 2 in rabbit afferent arterioles induced potent vasoconstrictions that were abolished with the superoxide dismutase mimetic 4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl (tempol), and potentiated with L-NAME (78), suggesting that endothelial TXA 2 R activation induces O 2 Ϫ -mediated vasoconstrictions that are "buffered" with NO.…”

“…We propose that the primed states of the NO-and Ca 2ϩ -sensitizing pathways place the basal contractile state on the early phases of their sigmoid response curves, with respect to TXA 2 signaling, such that changes in either vasoconstrictive or vasorelaxant signaling can produce rapid, but subtly buffered, contractile or relaxant responses; thus, maintaining the highly responsive homeostatic cerebral blood flow within a narrow range in the face of changes is systemic blood pressure (79). Interestingly, cerebrovascular TXA 2 (80) and NO (76) production are greater than in other arteries, such as the aorta, lending further support that the basal cerebrovascular contractile state is tightly controlled.…”