<b>Different effect of serotonin on intracellular calcium ion dynamics in the smooth muscle cells between rat posterior ciliary artery and vorticose </b><b>vein </b>

Abstract

5-hydroxytriptamine (5-HT: serotonin) is an important transmitter that causes vessel constriction, although few studies have examined the effect of 5-HT on venous smooth muscles. The intracellular Ca 2+ concentration ([Ca 2+ ] i ) plays an essential role in stimulus-response coupling in numerous tissue/cells including vascular smooth muscle cells. The present study was performed to examine whether differences between arteries and veins in the response to 5-HT can be detected under confocal microscope with respect to [Ca 2+ ] i dynamics. In posterior ciliary arteries of rats, 5-HT induced a [Ca 2+ ] i increase. The 5-HT-induced responses were caused by both Ca 2+ influx and mobilization. Agonist and antagonist experiments revealed that arterial smooth muscles possess 5-HT 1a, 1b, 2 (Gprotein-coupled type) and 5-HT 3 (ion channel type) receptors, and that 5-HT 2 in particular plays a major role in these responses. For vorticose veins, the 5-HT-induced responses were also caused by both Ca 2+ influx and mobilization. However, the cAMP dependent pathway (5-HT 4-7 ) was found to be significant in vasocontraction with respect to 5-HT in these vessels. Thus, Ca 2+ mobilization was induced by 5-HT 2 and 5-HT 4-7 in a vessel-dependent manner, whereas Ca 2+ influx universally was induced by 5-HT 3 . These results indicate that the posterior ciliary arteries and vorticose veins in the same tissue might differ greatly in their responses to stimulus.Retinal vein occlusion is the second most common retinal vascular disorder after diabetic retinopathy and is considered to be an important cause of visual impairment (9, 54). Ischemic disorders of the optic nerve constitute an important cause of visual loss (7, 30). For example, ischemic optic neuropathy, an acute disorder of the optic nerve, is now known to be a common yet serious vision-threatening disease in middle-aged and elderly populations (13,72). Similarly, evidence is mounting that vascular insufficiency in the intraorbital portion of the optic nerve might play an important role in amorose glaucomatous optic neuropathy and papilloedema (65, 83). The main vascular sources of the intraorbital portion of the optic nerve consist of the branches of the posterior ciliary artery and the central retinal artery (29,36,50,79). The choroid blood vessels of the eye provide 80-95% of the blood to the ocular structures including the outer retina and ciliary processes (6). The central retinal artery supplies the optic nerve and the inner retina, while the posterior ciliary artery pierces the sclera to enter the choroidal coat of the eye. The central retinal artery ends without significant anastomoses (32). The choroidal vessels are innervated by sympathetic and parasympathetic nerves; the parasympathetic innervation of the choroid derives from the ipsilateral pterygopalatine ganglion (59). Parasympathetic nerve stimulation produces nitric oxide-mediated vasodilation, which

Platelet Serotonin Aggravates Myocardial Ischemia/Reperfusion Injury via Neutrophil Degranulation

“…However, serotonin has been shown to stimulate Ca 2+ influx and intracellular Ca 2+ mobilization in vascular smooth muscle cells both via G protein coupled/IP 3 -dependent (eg, 5-HT 2 receptor subset) and cAMP/PKA-dependent (eg, 5-HT 4-7 receptor subsets) signaling pathways. 18,47 We demonstrated that serotonin stimulated neutrophil degranulation via the receptor subtype 7 in humans.…”

“…For in vitro stimulation, blood was incubated with either vehicle, or 100 µmol/L 5-hydroxytryptamine (5-HT, serotonin; Sigma-Aldrich CHEMIE, Steinheim, Germany) for 15 minutes, as previously described. [15][16][17][18] Platelet rich plasma (PRP) was prepared as described above. Samples were diluted 1:6 in 37°C warm PBS.…”