scholarly journals Cardioprotective Properties of Opioid Receptor Agonists in Rats With Stress-Induced Cardiac Injury

2019 ◽  
pp. 375-384
Author(s):  
E. PROKUDINA ◽  
L MASLOV ◽  
N. NARYZHNAYA ◽  
S. TSIBULNIKOV ◽  
Y. LISHMANOV ◽  
...  
Keyword(s):  
Opioid Receptor ◽  
Wistar Rats ◽  
Immobilization Stress ◽  
Cardiac Injury ◽  
Endogenous Opioids ◽  
Heart Injury ◽  
Mr 2266 ◽  
Opioid Receptor Agonists ◽  
Stimulation Of

The objectives of this study were to investigate the role of endogenous opioids in the mediation of stress-induced cardiomyopathy (SIC), and to evaluate which opioid receptors regulate heart resistance to immobilization stress. Wistar rats were subjected to 24 h immobilization stress. Stress-induced heart injury was assessed by 99mTc-pyrophosphate accumulation in the heart. The opioid receptor (OR) antagonists (naltrexone, NxMB – naltrexone methyl bromide, MR 2266, ICI 174.864) and agonists (DALDA, DAMGO, DSLET, U-50,488) were administered intraperitoneally prior to immobilization and 12 h after the start of stress. In addition, the selective µ OR agonists PL017 and DAMGO were administered intracerebroventricularly prior to stress. Finally pretreatment with guanethidine was used. Naltrexone did not alter the cardiac 99mTc-PP accumulation in stressed rats. NxMB aggravated stress-induced cardiomyopathy (P=0.005) (SIC). The selective µ OR agonist DALDA, which does not cross the blood-brain barrier, completely prevented (P=0.006) SIC. The µ OR agonist DAMGO exhibited weaker effect than DALDA. The selective δ ligand (DSLET) and κ OR ligand (U-50,488) did not alter stress-induced 99mTc-pyrophosphate accumulation in the heart. Intracerebroventricular administration of the µ OR agonists aggravated SIC. Pretreatment with guanethidine abolished this effect (P=0.01). Guanethidine alone exhibited cardioprotective properties. A stimulation of central µ OR promotes an appearance of SIC. In contrast, stimulation of peripheral µ OR contributes to an increase in cardiac tolerance to stress.

scholarly journals Intrahypothalamic Angiogenesis Induced by Osmotic Stimuli Correlates with Local Hypoxia: A Potential Role of Confined Vasoconstriction Induced by Dendritic Secretion of Vasopressin

Endocrinology ◽  
2008 ◽  
Vol 149 (9) ◽  
pp. 4279-4288 ◽  
Author(s):  
Gérard Alonso ◽  
Evelyne Gallibert ◽  
Chrystel Lafont ◽  
Gilles Guillon
Keyword(s):  
Wistar Rats ◽  
Vascular Endothelial ◽  
Magnocellular Neurons ◽  
Axon Terminals ◽  
Magnocellular Nuclei ◽  
Osmotic Stimulation ◽  
Osmotic Stimulus ◽  
Endothelial Growth Factor ◽  
Stimulation Of

We have previously shown that hyperosmotic stimulation of adult Wistar rats induces local angiogenesis within hypothalamic magnocellular nuclei, in relation to the secretion of vascular endothelial growth factor (VEGF) by the magnocellular neurons. The present study aimed at understanding how osmotic stimulus relates to increased VEGF secretion. We first demonstrate a correlation between increased VEGF secretion and local hypoxia. Osmotic stimulation is known to stimulate the metabolic activity of hypothalamic magnocellular neurons producing arginine vasopressin (AVP) and to increase the secretion of AVP, both by axon terminals into the circulation and by dendrites into the extracellular space. In AVP-deficient Brattleboro rats, the dramatic activation of magnocellular hypothalamic neurons failed to induce hypoxia, VEGF expression, or angiogenesis, suggesting a major role of hypothalamic AVP. A possible involvement of dendritic AVP release is supported by the findings that 1) hypoxia and angiogenesis were not observed in non osmotically stimulated Wistar rats in which circulating AVP was increased by the prolonged infusion of exogenous AVP, 2) contractile arterioles afferent to the magnocellular nuclei were strongly constricted by the perivascular application of AVP via V1a receptors (V1a-R) stimulation, and 3) after the intracerebral or ip administrations of selective V1a-R antagonists to osmotically stimulated rats, hypothalamic hypoxia and angiogenesis were or were not inhibited, respectively. Together, these data strongly suggest that the angiogenesis induced by osmotic stimulation relates to tissue hypoxia resulting from the constriction of local arterioles, via the stimulation of perivascular V1a-R by AVP locally released from dendrites.

Regulation of plasma motilin by opioids in the dog

1989 ◽  
Vol 257 (1) ◽  
pp. G41-G45
Author(s):  
P. Poitras ◽  
M. Boivin ◽  
R. G. Lahaie ◽  
L. Trudel
Keyword(s):  
Opioid Receptor ◽  
Contractile Activity ◽  
Endogenous Opioids ◽  
Phase Iii ◽  
Endogenous Opiates ◽  
Small Intestinal Motility ◽  
Opioid Administration ◽  
Small Intestinal ◽  
Plasma Motilin ◽  
Opioid Receptor Agonists

In the first part of this study, we compared the effects of morphine and trimebutine, two opioid receptor agonists, on small intestinal motility and plasma motilin in dogs. Morphine (100 micrograms/kg iv for 10 min) induced first a typical vomiting myoelectric profile followed subsequently by a migrating electrical activity mimicking phase III of the migrating myoelectric complex; trimebutine (5 mg/kg iv for 10 min) initiated only a migrating phase III-like activity. Despite their different initial contractile effects, both agents induced a significant and similar rise in plasma motilin that preceded the beginning of the premature phase III. In the second portion of the study, naloxone, an opioid receptor antagonist, was infused to verify the influence of endogenous opiates on plasma motilin and on the migrating motor complex. Naloxone (2 mg/kg, then 0.5 mg.kg-1.h-1 iv) delayed significantly the cyclic recurrence of plasma motilin peak increases and of the phase IIIs. In some animals, where naloxone abolished the phase IIIs, the amplitude of the motilin peak increases was significantly diminished. These results suggest 1) that opioid administration increases plasma levels of motilin by a mechanism that is independent of the intestinal contractile activity, and 2) that endogenous opioids could be physiological inducers of plasma motilin increases in the conscious dog.

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