Augmented Responses to 5-HT2-Receptor-Mediated Vasoconstrictions in Atherosclerotic Rabbit Common Carotid Arteries

Fujiwara, Toshimasa; Chiba, Shigetoshi

doi:10.1097/00005344-199509000-00023

Cited by 8 publications

(2 citation statements)

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“…Still, in previous investigations on the isolated rabbit carotid artery it was reported that only 5-HT 2 receptors were involved in contractions induced by serotonin [21, 22]. Accordingly, in our investigation ketanserin (a 5-HT 2 receptor antagonist) abolished contractile response of the rat carotid artery to serotonin.…”

Section: Discussioncontrasting

confidence: 37%

Contribution of Thromboxane A2 in Rat Common Carotid Artery Response to Serotonin

Radenković

Stojanović²,

Topalović³

2010

Sci. Pharm.

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Serotonin is a vasoactive substance that in different blood vessels mostly induces vasoconstriction. Considering the important role of common carotid artery in brain blood supply, the aims of this study were to investigate the effect of serotonin on isolated rat common carotid artery and also to examine participation of intact endothelium, cyclooxygenase products, Ca++ channels and 5-HT2 receptors in serotonin-evoked action. Endothelium was mechanically removed from some vascular rings. Circular artery segments were placed in organ baths containing Krebs–Ringer bicarbonate solution. Cumulative concentration-contraction curves for serotonin were obtained in rings previously equilibrated at basal tone. Serotonin produced concentration-dependent contraction, which was unaltered by endothelial denudation. Serotonin-induced effect was notably and comparably reduced by indomethacin (cyclooxygenase inhibitor) or OKY–046 (thromboxane A2-synthase inhibitor) on intact or denuded rings. Nifedipine (Ca++ channel blocker) or ketanserin (5-HT2 receptor antagonist) strongly reduced serotonin-evoked effect. Our results suggest that serotonin produced concentration-dependent and endothelium-independent contraction of carotid artery, which was initiated by activation of 5-HT2 receptors located on smooth muscle cells and mediated via L-type Ca++ channels. Thromboxane A2 from smooth muscle cells notably contributed to the overall contraction of carotid artery induced by serotonin.

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Section: Discussioncontrasting

confidence: 37%

Contribution of Thromboxane A2 in Rat Common Carotid Artery Response to Serotonin

Radenković

Stojanović²,

Topalović³

2010

Sci. Pharm.

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“…UK, unknown receptor mechanism. Data were collected from the following references: Lemberger et al, 1984;Miller et al, 1984;Feniuk et al, 1985;Nyborg and Mikkelsen, 1985;Cohen, 1986;Leff et al, 1987;Hamel et al, 1989Hamel et al, , 1993Parsons et al, 1989Parsons et al, , 1992Bodelsson et al, 1990;Borton et al, 1990;Chester et al, 1990;Gaw et al, 1990;Mylecharane, 1990;Toda and Okamura, 1990;van Heuven-Nolsen et al, 1990;Asher et al, 1991;Lai et al, 1991;Parsons, 1991;Sumner, 1991;Cohen, 1992a,b, 1993;Dorigo et al, 1992;Eglen et al, 1992;Weiner et al, 1992;Bax et al, 1993;Glusa and Mü ller-Schweinitzer, 1993;Jansen et al, 1993;Cushing et al, 1994Cushing et al, , 1996Yildiz and Tuncer, 1994;Fujiwara and Chiba, 1995;Miranda et al, 1995;Schmuck et al, 1996;Terrón, 1996;Valentin et al, 1996;Verheggen et al, 1996Verheggen et al, , 1998Verheggen et al, , 2004Verheggen et al, , 2006Zwaveling et al, 1996;…”

Section: Figmentioning

confidence: 99%