Effects of paroxetine on cardiovascular response to mental stress in subjects with a history of coronary artery disease and no psychiatric diagnoses

Golding, Michael; Kotlyar, Michael; Carson, Stanley W.; Hoyler, Sherri; Lazarus, Cindy; Davidson, Charles S.; Guzzo, Joseph; Sontz, Eric; Garbutt, James C.

doi:10.1007/s00213-005-0075-7

Cited by 21 publications

(19 citation statements)

References 24 publications

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“…Interestingly, prosencephalic activation of the 5-HT3 agonist receptor exerts an inhibitory action on the pressor part of the baroreflex function [10]. Healthy individuals with family histories of coronary arterial disease receiving PAR treatment presented with lower blood pressure during psychosocial stress tests, suggesting a cardio-protective effect [20]. Using SSRI to control panic syndrome in humans seems to be beneficial to the heart by increasing heart rate variability [9].…”

Section: Discussionmentioning

confidence: 99%

Antidepressant treatment decreases daily salt intake and prevents heart dysfunction following subchronic aortic regurgitation in rats

Gobbi

Omoto

Siqueira

et al. 2015

Physiology & Behavior

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Depression is a predictor of poor prognosis in patients with heart failure. Selective serotonin (5-HT) reuptake inhibitors (SSRIs) may improve these outcomes. Left ventricular volume overload induced hypertrophy that is associated with aortic regurgitation (AR) leads to ventricular dysfunction and heart failure. The aim of this study was to verify the effects of the SSRI paroxetine on cardiac function, as well as on fluid intake and excretion, in subchronic AR. Male Wistar rats (260 to 280g) received sham (SH) surgery or AR induced by retrograde puncture of the aortic valve leaflets. The presence of AR was confirmed by echocardiography (ECHO) exams. Four weeks after AR surgery, subcutaneous injections of paroxetine (PAR: 10mg/kg 3 times in a week) or saline were administered. The rats were randomly divided into the following 4 groups and treated for 4 weeks: AR-PAR, ARsaline, SH-PAR and SH-saline. At the end of the treatment period, fractional shortening was preserved in AR-PAR, compared to AR-saline (46.6±2.7% vs 38.3±2.2%, respectively). Daily 0.3 M NaCl intake was reduced in PAR-treated rats. Natriuresis was increased in weeks 2-3 after PAR treatment. Our results suggest that augmentation of central 5-HT neurotransmission has a beneficial effect on cardiovascular remodeling following volume overload. The mechanisms underlying this effect are unknown.

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Section: Discussionmentioning

confidence: 99%

Antidepressant treatment decreases daily salt intake and prevents heart dysfunction following subchronic aortic regurgitation in rats

Gobbi

Omoto

Siqueira

et al. 2015

Physiology & Behavior

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“…11,34 A study of 4 weeks of paroxetine therapy in 8 healthy subjects resulted in a 10%–15% reduction in SBP and DBP responses to mental stress relative to measures obtained while participants were receiving placebo. 10 …”

Section: Discussionmentioning

confidence: 99%

“…However, recent evidence suggests that selective serotonin reuptake inhibitors (SSRIs) may reduce mental-stress-induced hemodynamic response, metabolic risk factors, 10,11 and platelet activity. 12,13 We therefore conducted the Responses of Mental Stress Induced Myocardial Ischemia to Escitalopram Treatment (REMIT) trial (NCT00574847) to investigate whether SSRI treatment can improve MSIMI.…”

Section: Introductionmentioning

confidence: 99%

Effect of Escitalopram on Mental Stress–Induced Myocardial Ischemia

Jiang¹,

Velázquez²,

Kuchibhatla³

et al. 2013

JAMA

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“…SSRIs have several physiological effects, as evidenced by studies indicating that in non-depressive individuals, SSRIs can decrease sympathetic nervous system activity at rest (as indicated by reduced plasma norepinephrine concentrations) and during mental stress tasks (as measured by lowered heart rate, blood pressure, and plasma catecholamine concentrations) (18,19,43). Moreover, SSRIs reportedly decreased platelet activation in patients treated for depression and in healthy volunteers (1,34,40,41).…”

Section: Discussionmentioning

confidence: 99%

σ₁-Receptor stimulation with fluvoxamine ameliorates transverse aortic constriction-induced myocardial hypertrophy and dysfunction in mice

Tagashira

Bhuiyan

Shioda

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

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Selective serotonin reuptake inhibitors (SSRIs) are known to reduce post-myocardial infarction-induced morbidity and mortality. However, the molecular mechanism underlying SSRI-induced cardioprotection remains unclear. Here, we investigated the role of σ1-receptor (σ1R) stimulation with fluvoxamine on myocardial hypertrophy and cardiac functional recovery. Male ICR mice were subjected to transverse aortic constriction (TAC) in the cardiac aortic arch. To confirm the cardioprotective role of fluvoxamine by σ1R stimulation, we treated mice with fluvoxamine (0.5 or 1 mg/kg) orally once per day for 4 wk after the onset of aortic banding. Interestingly, in untreated mice, σ1R expression in the left ventricle (LV) decreased significantly over the 4 wk as TAC-induced hypertrophy increased. In contrast, fluvoxamine administration significantly attenuated TAC-induced myocardial hypertrophy concomitant with recovery of σ1R expression in the LV. Fluvoxamine also attenuated hypertrophy-induced impaired LV fractional shortening. The fluvoxamine cardioprotective effect was nullified by treatment with a σ1R antagonist [NE-100 (1 mg/kg)]. Importantly, another SSRI with very low affinity for σ1Rs, paroxetine, did not elicit antihypertrophic effects in TAC mice and cultured cardiomyocytes. Fluvoxamine treatment significantly restored TAC-induced impaired Akt and endothelial nitric oxide synthase (eNOS) phosphorylation in the LV. Our findings suggest that fluvoxamine protects against TAC-induced cardiac dysfunction via upregulated σ1R expression and stimulation of σ1R-mediated Akt-eNOS signaling in mice. This is the first report of a potential role for σ1R stimulation by fluvoxamine in attenuating cardiac hypertrophy and restoring contractility in TAC mice.

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Effects of paroxetine on cardiovascular response to mental stress in subjects with a history of coronary artery disease and no psychiatric diagnoses

Abstract: Paroxetine has antihypertensive properties during periods of psychological stress in psychiatrically healthy subjects with a history of CAD, and so should be evaluated for potential cardio-protective qualities.

Cited by 21 publications

References 24 publications

Antidepressant treatment decreases daily salt intake and prevents heart dysfunction following subchronic aortic regurgitation in rats

Antidepressant treatment decreases daily salt intake and prevents heart dysfunction following subchronic aortic regurgitation in rats

Effect of Escitalopram on Mental Stress–Induced Myocardial Ischemia

σ₁-Receptor stimulation with fluvoxamine ameliorates transverse aortic constriction-induced myocardial hypertrophy and dysfunction in mice

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Effects of paroxetine on cardiovascular response to mental stress in subjects with a history of coronary artery disease and no psychiatric diagnoses

Abstract: Paroxetine has antihypertensive properties during periods of psychological stress in psychiatrically healthy subjects with a history of CAD, and so should be evaluated for potential cardio-protective qualities.

Cited by 21 publications

References 24 publications

Antidepressant treatment decreases daily salt intake and prevents heart dysfunction following subchronic aortic regurgitation in rats

Antidepressant treatment decreases daily salt intake and prevents heart dysfunction following subchronic aortic regurgitation in rats

Effect of Escitalopram on Mental Stress–Induced Myocardial Ischemia

σ1-Receptor stimulation with fluvoxamine ameliorates transverse aortic constriction-induced myocardial hypertrophy and dysfunction in mice

Contact Info

Product

Resources

About

σ₁-Receptor stimulation with fluvoxamine ameliorates transverse aortic constriction-induced myocardial hypertrophy and dysfunction in mice