Opioid Peptide Modulation of Circulatory and Endocrine Response to Mental Stress in Humans

Fontana, Fiorella; Bernardi, P; Pich, Emilio Merlo; Boschi, Stefano; Iasio, Rosaria De; Spampinato, Santi; Grossi, G.

doi:10.1016/s0196-9781(96)00319-1

Cited by 44 publications

(19 citation statements)

References 34 publications

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“…α-and β-Adrenergic blockades were reported to inhibit the formation of neointima after endothelial denudation of an artery in animal models (13,14), and the β-adrenergic blockade has a protective function against myocardial ischemic events, including plaque rupture, in humans (14). Besides these pathways, β-endorphin (END), an endogenous opioid, is also produced in the pituitary gland; it is released into the circulating blood to act as a relaxing factor against stress (15)(16)(17). However, little is known about the effects of endogenous opioids on the process of arteriosclerosis.…”

Section: Introductionmentioning

confidence: 99%

Immobilization Stress Inhibits Intimal Fibromuscular Proliferation in the Process of Arterial Remodeling in Rats

et al. 2008

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Section: Introductionmentioning

confidence: 99%

Immobilization Stress Inhibits Intimal Fibromuscular Proliferation in the Process of Arterial Remodeling in Rats

et al. 2008

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“…The lack of an influence of naloxone on cardiovascular responses in our study might be attributed to different dosage used. However, similar doses were used in many other studies, irrespective of the study design (10,13,14,16,25). Therefore, and because of effects on the HPA and HPG axis, it is rather unlikely that dosage might have been too low to detect an effect of naloxone on cardiovascular measures.…”

Section: Discussionmentioning

confidence: 98%

“…Two studies comparing stress responses between men and women have observed inconsistent results. In one study employing naloxone (16), no sex differences were noted, whereas another experiment (2) demonstrated blunted blood pressure responses to the opioid antagonist naltrexone in women compared with men. Despite these cardiovascular differences, similar responses in ACTH and cortisol were observed in women and men (2).…”

Section: Discussionmentioning

confidence: 99%

Naloxone does not influence cardiovascular responses to mild mental stress in postmenopausal women

Litschauer

Schaller

Wolzt

2005

American Journal of Physiology-Heart and Circulatory Physiology

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Litschauer, Brigitte, Georg Schaller, and Michael Wolzt. Naloxone does not influence cardiovascular responses to mild mental stress in postmenopausal women. Am J Physiol Heart Circ Physiol 289: H2120-H2125, 2005. First published July 1, 2005; doi:10.1152/ajpheart.01113.2004The interaction between central opioid activity, sex hormones, and the cardiovascular reactivity to stress is unknown. Twenty-eight healthy postmenopausal women, 16 without, and 12 with hormone replacement therapy (HRT) participated in this randomized, double-blind, cross-over study. The opioid receptor antagonist naloxone or placebo was administered intravenously on 2 different days and mild mental stress was induced by the Stroop Color-Word Test. Cardiovascular responses were assessed noninvasively by impedance cardiography. Stress significantly increased stroke volume, cardiac output, blood pressure, and heart rate, which was not influenced by opioid receptor blockade. Whereas naloxone increased cortisol plasma concentrations irrespective of HRT status, luteinizing hormone concentrations, which were higher in non-HRT compared with HRT women, were increased by naloxone in women with HRT only. These data suggest that the opioidergic tone of the hypothalamus-pituitary-adrenal axis persists in postmenopausal women, irrespective of HRT use, while the opioidergic tone on the hypothalamus-pituitary-gonadal axis seems to depend on an estrogenic milieu. Naloxone does not alter cardiovascular mental stress reactions in postmenopausal women independent of their hormone substitution status.hormone replacement therapy; reactivity; luteinizing hormone; cortisol THE INCIDENCE OF CARDIOVASCULAR diseases (CVD) is lower in premenopausal women compared with men, but this difference is no longer apparent after menopause. While large-scaled randomized trials (37, 42) failed to observe a reduction of cardiovascular events or indicated increased risk for CVD in women on hormone replacement therapy (HRT), several studies suggest a CVD risk reduction (5, 35) and a blood pressurelowering effect (26, 36) of estrogen or estrogen plus progestin HRT in postmenopausal women. Thus HRT and its impact on the cardiovascular system of women are under debate.Cardiovascular responses to mental stress are thought to contribute to the risk for hypertension and coronary atherosclerosis (21). Studies suggest that estrogens also modulate cardiovascular functions during stressful encounters, as premenopausal women are less reactive to psychosocial stressors compared with postmenopausal women and men (3, 31, 33) and estrogen treatment blunts pressor and neuroendocrine responses in postmenopausal women (20,24,27,40). Thus an increased reactivity to mental stress may contribute to the risk of cardiovascular morbidity and mortality after menopause.Endogenous opioids have been implicated in many regulatory functions. Studies have suggested a dampening role of the opioidergic system on cardiovascular stress responses. Activated by mental stress the central opioidergic system is supposed to...

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“…Plasma levels of immunoreactive (ir) ß-endorphinlike material were radioimmunoassayed after chromatographic pre-extraction as previously described [19]. The detection limit was 3 fmol/ml [mean ± S.D.…”

Section: 3hormone Assaysmentioning

confidence: 99%

β-Endorphin in pressor response to hyperventilation in elderly patients with essential and secondary hypertension

et al. 2008

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AbstractIt has been observed that a distinct blood pressure (BP) response to prolonged and forced hyperventilation in adult patients with essential hypertension is associated with significant changes in plasma catecholamine and β-endorphin levels. This paper investigated whether hemodynamic and neuro-endocrine responses to hyperventilation in elderly patients with essential hypertension (n = 39, mean age 81 ± 3 years) differ from those in elderly patients with secondary hypertension (isolated systolic hypertension, bilateral chronic nephropathy, nephroangiosclerosis, diabetic nephropathy and hyperparathyroidism) (n = 39, mean age 80 ± 1 years). Plasma β-endorphin levels were normal in patients with essential hypertension and increased in patients with secondary hypertension. Plasma norepinephrine levels were normal in both populations. Hyperventilation decreased BP and norepinephrine levels and increased β-endorphin levels in essential hypertensive patients, whereas it did not significantly change BP or neuro-hormonal levels in secondary hypertensive patients. Hierarchical cluster analysis based on BP response to hyperventilation disclosed a sub-group of essential hypertensive patients with the highest basal levels of norepinephrine and the lowest β-endorphin levels, in whom the BP decrease following hyperventilation was correlated with the decrease in norepinephrine and increase in β-endorphin levels. This suggests that b-endorphin may be involved in modulating sympatho-adrenergic activity in elderly patients with essential hypertension.

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Opioid Peptide Modulation of Circulatory and Endocrine Response to Mental Stress in Humans

Cited by 44 publications

References 34 publications

Immobilization Stress Inhibits Intimal Fibromuscular Proliferation in the Process of Arterial Remodeling in Rats

Immobilization Stress Inhibits Intimal Fibromuscular Proliferation in the Process of Arterial Remodeling in Rats

Naloxone does not influence cardiovascular responses to mild mental stress in postmenopausal women

β-Endorphin in pressor response to hyperventilation in elderly patients with essential and secondary hypertension

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