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Endogenous opioid peptides and mental stress in congestive heart failure patients

F Fontana1, P Bernardi, E M Pich

  • 1Dipartimento di Medicina Interna, Cardioangiologia, Epatologia, Ospedale S. Orsola, Bologna, Italy.

Peptides
|January 23, 1998
PubMed

Insights

In patients with congestive heart failure (CHF), stress increases certain hormones. Naloxone hydrochloride, an opioid antagonist, amplified these stress responses, suggesting the body

Area of Science:

  • Cardiology
  • Neuroendocrinology
  • Pharmacology

Background:

  • Patients with acute congestive heart failure (CHF) exhibit elevated levels of beta-endorphin, norepinephrine, atrial natriuretic factor (ANF), and endothelin-1.
  • The endogenous opioid system's role in modulating cardiovascular responses during stress in CHF is not fully understood.

Purpose of the Study:

  • To investigate the impact of blocking the endogenous opioid system with naloxone hydrochloride on hemodynamic and neuroendocrine responses to mental stress in CHF patients.
  • To determine if the endogenous opioid system attenuates the stress-induced release of norepinephrine and other hormones in CHF.

Main Methods:

  • Two groups of 10 patients each with New York Heart Association class III acute CHF underwent the Mental Arithmetic Test (MAT).
  • Patients were tested during placebo infusion and naloxone hydrochloride infusion.
  • Hemodynamic parameters (blood pressure, heart rate) and plasma levels of various peptides (Met-enkephalin, dynorphin B, beta-endorphin, norepinephrine, ANF, endothelin-1) were measured before and after the MAT.

Main Results:

  • The MAT significantly increased blood pressure, heart rate, and plasma levels of Met-enkephalin, dynorphin B, beta-endorphin, norepinephrine, ANF, and endothelin-1 during placebo infusion.
  • The increases in norepinephrine, ANF, and hemodynamic parameters following the MAT were significantly higher during naloxone hydrochloride infusion compared to placebo.
  • These findings suggest that the endogenous opioid system normally attenuates the hemodynamic response to stress in CHF patients by reducing norepinephrine release.

Conclusions:

  • The endogenous opioid system plays a significant role in modulating the cardiovascular and neuroendocrine responses to acute mental stress in patients with CHF.
  • Blocking opioid receptors with naloxone hydrochloride exacerbates the hemodynamic and hormonal responses to stress, indicating a protective role of the endogenous opioid system.
  • Targeting the endogenous opioid system may offer novel therapeutic strategies for managing stress-related cardiovascular dysfunction in CHF.

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