Effect of the activation of central 5-HT2C receptors by the 5-HT2C agonist mCPP on blood pressure and heart rate in rats

Ferreira, Hadla S.; Oliveira, Elenilda Farias de; Faustino, Thiallan Nery; Silva, Emilio de Castro e; Fregoneze, J.B.

doi:10.1016/j.brainres.2005.01.054

Cited by 15 publications

(7 citation statements)

References 36 publications

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“…That activation of these receptors elevates arterial pressure was convincingly demonstrated by Ferreira et al (2005): icv administration of selective 5-HT2C agonist mCPP elevated, in a dose-dependent manner, the mean arterial pressure (but not HR) in conscious rats, and this effect was completely prevented by central administration of the selective 5-HT2C antagonist SDZ SER 082. Importantly, the antagonist had no effect on the basal AP and HR, but greatly attenuated pressor, but not tachycardic response to the restraint stress.…”

Section: -Ht2c Receptors: Involvement In Stress-elicited Hypertension?mentioning

confidence: 93%

Central 5-HT receptors in cardiovascular control during stress

Nalivaiko

Sgoifo

2009

Neuroscience & Biobehavioral Reviews

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Section: -Ht2c Receptors: Involvement In Stress-elicited Hypertension?mentioning

confidence: 93%

Central 5-HT receptors in cardiovascular control during stress

Nalivaiko

Sgoifo

2009

Neuroscience & Biobehavioral Reviews

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“…Furthermore, microinjection of 8-hydroxy-DPAT, a 5-HT1A agonist, into the medullary raphe attenuates stress-induced tachycardic and pressor responses (Nalivaiko et al., 2005, Ngampramuan et al., 2008). Alternatively, central 5-HT2C receptors have been demonstrated to regulate, in large part, the pressor response during restraint stress in rats (Ferreira et al., 2005) in the nucleus tractus soliatrius. Furthermore, 5-HT3 receptors located within the sympathetic ganglia may likely regulate stress-induced hypertension (Alkadhi et al., 1996).…”

Section: Effect Of Neuroinflammation On Neurobiologic Substrates Undementioning

confidence: 99%

Neuroinflammation at the interface of depression and cardiovascular disease: Evidence from rodent models of social stress

Finnell

Wood

2016

Neurobiology of Stress

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A large body of evidence has emerged linking stressful experiences, particularly from one's social environment, with psychiatric disorders. However, vast individual differences emerge in susceptibility to developing stress-related pathology which may be due to distinct differences in the inflammatory response to social stress. Furthermore, depression is an independent risk factor for cardiovascular disease, another inflammatory-related disease, and results in increased mortality in depressed patients. This review is focused on discussing evidence for stress exposure resulting in persistent or sensitized inflammation in one individual while this response is lacking in others. Particular focus will be directed towards reviewing the literature underlying the impact that neuroinflammation has on neurotransmitters and neuropeptides that could be involved in the pathogenesis of comorbid depression and cardiovascular disease. Finally, the theme throughout the review will be to explore the notion that stress-induced inflammation is a key player in the high rate of comorbidity between psychosocial disorders and cardiovascular disease.

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“…The effect of the 5-HT 3 agents on blood pressure control shown in that study may be partially explained by their action on the septal area, since when the same serotonergic agents were administered in the medial septum/ vertical limb of the diagonal band complex (MS/vDB), 5-HT 3 receptors located in this area were also shown to exert a tonic sympathoinhibitory effect that seems to be mediated by an angiotensinergic-dependent mechanism (Urzedo-Rodrigues et al, 2011). Furthermore, it has also been shown that activation of central 5-HT 2C receptors induces hypertension in non-stressed rats and that the functional integrity of those receptors is essential for the rise in blood pressure that occurs in the course of restraint stress (Ferreira et al, 2005). The central opioid system also participates in blood pressure regulation (Bodnar, 2009;Feuerstein and Sirén, 1988).…”

Section: Introductionmentioning

confidence: 99%

Multiple opioid receptors mediate the hypotensive response induced by central 5-HT3 receptor stimulation

et al. 2011

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The aim of the present work was to investigate the role of brain μ, κ and δ opioid receptors in the central serotonergic mechanisms regulating blood pressure in rats. The data obtained show that: (1) pharmacological activation of central 5-HT(3) receptors yields a significant decrease in blood pressure; (2) the blockade of those receptors by a selective antagonist induces an acute hypertensive response; (3) the pharmacological blockade of central opioid receptors by three different opioid antagonists exhibiting variable degrees of selectivity to μ, κ and δ opioid receptors always suppressed the hypotensive response induced by central 5-HT(3) receptor stimulation; (4) the blockade of opioid receptors by the same opioid antagonists that impaired the hypotensive effect of central 5-HT(3) receptor stimulation failed to modify blood pressure in animals not submitted to pharmacological manipulations of central 5-HT(3) receptor function. It is shown that a 5-HT(3) receptor-dependent mechanism seems to be part of the brain serotonergic system that contributes to cardiovascular regulation since the hypertensive response observed after ondansetron administration indicates that central 5-HT(3) receptors exert a tonic inhibitory drive on blood pressure. Furthermore, the data obtained here clearly indicate that the hypotensive response observed after pharmacological stimulation of central 5-HT(3) receptors depends on the functional integrity of brain μ, κ and δ opioid receptors, suggesting that a functional interaction between serotonergic and opiatergic pathways in the brain is part of the complex, multifactorial system that regulates blood pressure in the central nervous system.

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Effect of the activation of central 5-HT2C receptors by the 5-HT2C agonist mCPP on blood pressure and heart rate in rats

Cited by 15 publications

References 36 publications

Central 5-HT receptors in cardiovascular control during stress

Central 5-HT receptors in cardiovascular control during stress

Neuroinflammation at the interface of depression and cardiovascular disease: Evidence from rodent models of social stress

Multiple opioid receptors mediate the hypotensive response induced by central 5-HT3 receptor stimulation

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