Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A biotinylated oligonucleotide probe was used to demonstrate the presence in the heart of the portion of the proopiomelanocortin messenger RNA which contains the sequence for beta-endorphin. The probe indicated the presence of beta-endorphin messenger RNA in cardiac tissue and specifically in the cardiac muscle cell. The probe also confirmed the well-documented presence of messenger RNA for beta-endorphin in the anterior and neurointermediate lobes of the pituitary. These findings indicate that in addition to the pituitary, beta-endorphin is produced in situ in the heart.
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PMID:Demonstration by in situ hybridization of the proopiomelanocortin gene in the rat heart. 159

The effect of intravenous administration of the opioid antagonist naloxone in rats with acute left coronary artery ligation was studied. The results demonstrated that naloxone in a dose 2 mg/kg b. w. affords its protection on infarcted animals by two mechanisms: Reduces by 22% the incidence of early arrhythmias that occur within 15-20 minutes of acute myocardial ischaemia, and are responsible for the early (up to the 30th minutes) postligation death; Reverses the hypotension that results from the development of cardiogenic shock after 30 minutes myocardial infarction. The total mortality after naloxone treatment was significantly reduced by 22%. Naloxone does not influence significantly the size of the infarcted area but the incidence of left ventricle wall perforations was decreased by 38%. Both effects of naloxone are attributed to the antagonism of opioid receptors either directly on the myocardium or through blocking the central action of beta-endorphin. A direct effect of naloxone on the cardiac muscle action potential cannot be excluded.
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PMID:Opioid peptides in experimental myocardial infarction. I. The effect of naloxone. 361 53

Research has suggested that exogenous opioid substances can have direct effects on cardiac muscle or influence neurotransmitter release via presynaptic modulation of neuronal inputs to the heart. In the present study, multiple-labelling immunohistochemistry was employed to determine the distribution of endogenous opioid peptides within the guinea-pig heart. Approximately 40% of cardiac ganglion cells contained immunoreactivity for dynorphin A (1-8), dynorphin A (1-17) and dynorphin B whilst 20% displayed leu-enkephalin immunoreactivity. Different populations of opioid-containing ganglion cells were identified according to the co-existence of opioid immunoreactivity with immunoreactivity for somatostatin and neuropeptide Y. Immunoreactivity for prodynorphin-derived peptides was observed in many sympathetic axons in the heart and was also observed, though to a lesser extent, in sensory axons. Leu-enkephalin immunoreactivity was observed in occasional sympathetic and sensory axons. No immunoreactivity was observed for met-enkephalin-arg-gly-leu or for beta-endorphin. These results demonstrate that prodynorphin-derived peptides are present in parasympathetic, sympathetic and sensory nerves within the heart, but suggest that only the prodynorphin gene is expressed in guinea-pig cardiac nerves. This study has shown that endogenous opioid peptides are well placed to regulate cardiac function via both autonomic and sensory pathways.
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PMID:Endogenous opioid peptides in parasympathetic, sympathetic and sensory nerves in the guinea-pig heart. 862 99

The activity of succinate dehydrogenase, pyruvate dehydrogenase and lactate dehydrogenase in homogenates from cardiac muscle, liver and brain of wild rodents inhabiting areas with high level of radioactivity (Komi Republic, Chernobyl NPP accident 30-km zone). There is a deficiency in pyruvate and succinate oxidation as well as the high rate of the lactate oxidation processes in organs of senescent wild rodents from radioactive polluted sites. The high level of lactate dehydrogenase activity in cardiac muscle and liver has been demonstrated in both young and senescent animals that is the aging process development evidence.
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PMID:[Age-dependant alterations of energy metabolism in rodents from radiation contaminated areas]. 1943 95