Peripheral 5-HT1D and 5-HT7 serotonergic receptors modulate sympathetic neurotransmission in chronic sarpogrelate treated rats

5-HT1D receptor inhibits renal sympathetic neurotransmission by nitric oxide pathway in anesthetized rats

“…5-HT seems to modulate adrenergic neurotransmission, leading to sympatho-excitatory or sympatho-inhibitory effects, and, consequently, into vasopressor and tachycardic or vasodepressor and bradycardic responses, respectively [9,13,15,16]. In this sense, some studies by our research team and others have suggested that 5-HT 1 receptor mediates inhibition of the sympathetic neurotransmission [9][10][11][12][13]17,18].…”

“…The dose of each antagonist was selected after consideration of our previous experience [13,[21][22][23].…”

“…The doses of all drugs (referring to their free base) were chosen on the basis of our previous experience [9,[11][12][13]15], and taking into account that i) for agonists, the criterion chosen was their pKs, while ii) for antagonists, the doses are always chosen to obtain a minimum of 50% degree of inhibition of the maximum effect evaluated in each experiment: in our experiments, the antagonists reverse the inhibition induced by L-694,247 on the pressor responses induced by electrical stimulation (see Figs. 6 and 7).…”

“…Thus, a potential therapeutical target would be the modulation of NE release after increased sympathetic activity; in this line, it has been established that NE release could be regulated by prejunctional receptors, including serotonin receptors [9][10][11][12][13][14]. 5-HT seems to modulate adrenergic neurotransmission, leading to sympatho-excitatory or sympatho-inhibitory effects, and, consequently, into vasopressor and tachycardic or vasodepressor and bradycardic responses, respectively [9,13,15,16].…”

“…5-HT seems to modulate adrenergic neurotransmission, leading to sympatho-excitatory or sympatho-inhibitory effects, and, consequently, into vasopressor and tachycardic or vasodepressor and bradycardic responses, respectively [9,13,15,16]. In this sense, some studies by our research team and others have suggested that 5-HT 1 receptor mediates inhibition of the sympathetic neurotransmission [9][10][11][12][13]17,18]. Despite the above findings along with the importance of the renal sympathetic neurotransmission in many cardiovascular diseases, the following, unfortunately, have not yet been determined: i) the effect of serotonin, the endogenous ligand, on the renal noradrenergic neurotransmission and the pharmacological nature of 5-HT receptors involved; ii) the effect of 5-HT 1 receptor subtype agonists on renal sympathetic outflow; and iii) the prejunctional or postjunctional nature of receptors implicated and the possible indirect pathways associated.…”