Mechanisms Involved in Serotonin-Induced Vasodilatation

Abstract

In vitro investigations have identified three major mechanisms which could contribute to the vasodilator action of serotonin (5-hydroxytryptamine, 5-HT): direct vascular smooth muscle relaxation; prejunctional inhibition of noradrenaline release from vascular sympathetic nerve terminals; and release of endothelium-derived relaxing factor (EDRF). In vivo studies have shown that in pig and cat common carotid circulations, rabbit hind-quarter and mesenteric circulations, and rat systemic vasculature, direct vascular smooth muscle relaxation may be the predominant mechanism involved, but the contribution of EDRF release remains to be established. In other circulations in vivo (dog femoral and common carotid), prejunctional inhibition of vascular sympathetic tone is the predominant mechanism responsible for serotonin-induced vasodilatation. All of these actions are mediated by 5-HT₁-like receptors, but different subtypes seem to be involved in each of these mechanisms. The prejunctional inhibitory receptor has been the most studied; depending on the tissue, these subtypes may resemble 5-HT_1A, 5-HT_1B, 5-HT_1c or 5-HT_1D binding sites, or the contractile receptor in dog saphenous vein.

Serotonin and Blood Pressure Regulation

“…In the rat jugular vein and pulmonary artery and coronary arteries of rat and greyhound, 5-HT causes relaxation through activation of 5-HT 2B and 5-HT 7 receptors (Mylecharane, 1990;Mankad et al, 1991;Woodman and Dusting, 1994;Ellis et al, 1995;Glusa and Roos, 1996;Centurión et al, 2000Centurión et al, , 2004Jähnichen et al, 2005). 5-HT relaxes human umbilical arteries (Haugen et al, 1997) and dilates skeletal muscle arterioles, an important finding with respect to blood pressure (Alsip and Harris, 1992;Alsip et al, 1996).…”

“…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;…”

Effect of cold storage in University of Wisconsin solution on the responses of porcine hepatic arteries to 5‐hydroxytryptamine and bradykinin in vitro

“…The inability of L-NOARG to inhibit significantly the relaxation responses to bradykinin is in contrast to its significantly inhibitory effect on the maximum relaxation response to 5-HT. The ability of L-NOARG to inhibit the relaxation response to 5-HT but not bradykinin may be due to (1) the different receptor systems stimulating the release of different endothelium-derived relaxing factors (EDRFs) (Boulanger et al, 1989;Hoeffner et al, 1989), (2) differences in the efficiency of receptor occupancy-effect coupling (Martin et al, 1992) and (3) (McKeown et al, 1988;Caldwell-Kenkel et al, 1989, 1990Holloway et al, 1990). These studies evaluated endothelial cell integrity of the microcirculation in whole perfused liver preparations using morphological and cytochemical indices.…”

Investigating Hemodynamic Responses to Electrical Neurostimulation

“…In the case of this depressor effect, presynaptic inhibition of NE from sympathetic nerve terminals occurs [177]. Normally, electrical stimulation, such as TENS, stimulates a vasoconstrictor response through the release of NE and ATP from postganglionic sympathetic neurons [178,179].…”

“…Serotonin decreases the calcium current through the channels. As a result, cytosolic levels of calcium decrease, causing inhibition of NE release from the sympathetic nerve terminal [177,181]. In addition, both serotonin and activation of α2…”