Central 5-HT receptors in cardiovascular control during stress

Nalivaiko, Eugene; Sgoifo, Andrea

doi:10.1016/j.neubiorev.2008.05.026

Cited by 41 publications

(22 citation statements)

References 90 publications

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“…We refer the reader to other reviews that cover different aspects of the CV system or that provide a more detailed historical perspective of 5-HT in the CV system: Kuhn et al, 1980;Marwood and Stokes, 1984;Docherty, 1988;Vanhoutte, 1991;van Zwieten et al, 1992;McCall and Clement, 1994;Yildiz et al, 1998;Nebigil and Maroteaux, 2001;Ramage, 2001;Doggrell, 2003;Côté et al, 2004;MaurerSpurej, 2005;Watts, 2005;Villalón and Centurión, 2007;Ramage and Villalón, 2008;Nalivaiko and Sgoifo, 2009;Nichols, 2009;Nigmatullina et al, 2009;Monassier et al, 2010;and Mercado et al, 2011. We will not discuss pulmonary blood pressure or pulmonary hypertension, but refer readers to an excellent review: MacLean and Dempsie, 2009.…”

Section: -Hydroxytryptamine (5-ht;mentioning

confidence: 99%

Serotonin and Blood Pressure Regulation

et al. 2012

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Section: -Hydroxytryptamine (5-ht;mentioning

confidence: 99%

Serotonin and Blood Pressure Regulation

et al. 2012

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“…Furthermore, 5-HT3 receptors located within the sympathetic ganglia may likely regulate stress-induced hypertension (Alkadhi et al., 1996). 5-HT central control of stress-induced cardiovascular responses is highly complex and has been thoroughly reviewed by (Nalivaiko and Sgoifo, 2009). Taken together, inflammation has demonstrated ability to alter the 5-HT system in the brain, and is therefore yet another inflammation-sensitive neurotransmitter that has the capacity to promote comorbidity between depression and CVD either through altered receptor activation or shifts in tryptophan catabolism via the IDO/kynurenine pathway.…”

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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“…Importantly, it has been demonstrated that chronic social defeat downregulates the 5-HT 1A receptor in the rat brain (Kieran et al, 2010). The 5-HT 1A receptors play an important role in inhibiting sympathetic neurons located in the medullary raphe area that activates the heart during stress (Nalivaiko, 2006; Nalivaiko and Sgoifo, 2009). In addition to sympathoinhibition, activation of 5-HT 1A receptors may have vagomimetic effects (Ngampramuan et al, 2008; Dutschmann et al, 2009; Carnevali et al, 2012a).…”

Section: Effects Of Stress and Psychosocial Factors On Vagal Modulatimentioning

confidence: 99%

Vagal modulation of resting heart rate in rats: the role of stress, psychosocial factors, and physical exercise

Carnevali

Sgoifo

2014

Front. Physiol.

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In humans, there are large individual differences in the levels of vagal modulation of resting heart rate (HR). High levels are a recognized index of cardiac health, whereas low levels are considered an important risk factor for cardiovascular morbidity and mortality. Several factors are thought to contribute significantly to this inter-individual variability. While regular physical exercise seems to induce an increase in resting vagal tone, chronic life stress, and psychosocial factors such as negative moods and personality traits appear associated with vagal withdrawal. Preclinical research has been attempting to clarify such relationships and to provide insights into the neurobiological mechanisms underlying vagal tone impairment/enhancement. This paper focuses on rat studies that have explored the effects of stress, psychosocial factors and physical exercise on vagal modulation of resting HR. Results are discussed with regard to: (i) individual differences in resting vagal tone, cardiac stress reactivity and arrhythmia vulnerability; (ii) elucidation of the neurobiological determinants of resting vagal tone.

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Central 5-HT receptors in cardiovascular control during stress

Cited by 41 publications

References 90 publications

Serotonin and Blood Pressure Regulation

Serotonin and Blood Pressure Regulation

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

Vagal modulation of resting heart rate in rats: the role of stress, psychosocial factors, and physical exercise

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