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

An improved radio-immunoassay using an antiserum directed towards the N-terminal part of the endogenous opioid peptide beta-endorphin 1-31 (beta-EP) was validated and applied to a study of beta-EP in plasma during ischaemic pain. Experimental ischaemic pain induced in seven healthy volunteers by the submaximal effort tourniquet test did not change plasma beta-EP or adrenocorticotrophin. Plasma beta-EP was determined in 21 patients with acute myocardial infarction (AMI) and in seven patients with unstable angina pectoris. Plasma beta-EP was 4.9 fmol/ml with 95% confidence limits, 3.2-7.8 fmol/ml in AMI patients at admittance, and 2.9 (2.0-3.4) fmol/ml one week later in stable and pain-free condition (p less than 0.05). The level in 49 healthy persons was 2.8 (2.4-2.9) fmol/ml. Elevated beta-EP levels were found in five AMI patients with cardiogenic shock and in four AMI patients dying within 24 h after admittance compared to the rest of AMI patients (p less than 0.02). beta-EP was not elevated during unstable angina pectoris, although pain scores were similar to AMI. The AMI group revealed a significant, although weak, positive correlation between plasma beta-EP and pain score (Spearman r = 0.49, p less than 0.05), while there was no correlation during unstable angina pectoris. beta-EP was not correlated to the amount of morphine required within the 48 h after admittance of AMI patients. We conclude that the increase of beta-EP in plasma during AMI may be due to stressful factors other than ischaemic pain and that it is questionable whether beta-EP in plasma is related to antinociception.
 ...
PMID:Plasma beta-endorphin during clinical and experimental ischaemic pain. 296 68

We tested the idea that cytokine antagonists are released during acute myocardial ischemia to counteract proinflammatory effects of cytokines. We investigated changes in plasma concentrations of the anticytokine molecules alpha-melanocyte-stimulating hormone (alpha-MSH), interleukin-1 receptor antagonist (IL-1ra), and soluble tumor necrosis factor receptor (sTNFr) in patients with acute myocardial infarction (AMI) or unstable angina (UA). Blood samples were collected at presentation in the coronary care unit, at 3-hour intervals for 24 hours, and daily for 4 days thereafter. There were no significant differences in the concentrations of cytokine antagonists in patients with AMI or UA. However, whereas concentrations of alpha-MSH were increased in early samples of patients with AMI or UA who were treated with a thrombolytic agent, they were consistently low in untreated patients. IL-1ra concentrations likewise were greater 3 and 6 hours after treatment in patients who underwent thrombolysis, whereas there was no significant difference in plasma sTNFr between the two groups. We suggest that during myocardial ischemia and thrombolysis anticytokine molecules released from the injured myocardium become available to reduce inflammation caused by cytokines and other mediators of inflammation.
 ...
PMID:Endogenous cytokine antagonists during myocardial ischemia and thrombolytic therapy. 763 97

Chronic stress and probably the accompanying changes in personal behaviours can influence life expectancy. The role of adrenocorticotropic hormone (ACTH) and cortisol in atherosclerosis is not widely accepted and incompletely characterized. Several reports support a role of these hormones in atherogenesis by modulating the function of vascular endothelium, the recruitment of circulating monocytes to the artery wall and their differentiation into macrophages- foam cells, by controlling the expression of pro- and anti-inflammatory interleukins. Previous reports suggested an important role of ACTH and cortisol in the modulation of atherosclerotic plaque progression by removal of excess free cholesterol from macrophages. Studies suggested a crucial role of these hormones on the development of acute coronary syndromes [(ACS); unstable angina, and acute myocardial infarction] and stroke, by modulating platelet aggregation and thrombus formation. This review focuses on the identified mechanisms and roles of ACTH and cortisol in atherogenesis, progression of atherosclerosis and the development of ACS. Finally, it proposes experimental studies to evaluate the therapeutic potential of new glucocorticoid antagonists, the effects that may derive from the inhibition cortisol synthesis and the role of 11beta-hydroxysteroid dehydrogenase type 1 inhibitors in atherogenesis, progression of atherosclerosis and the development of ACS. These hormones may be a possible additional target for the prevention and treatment of atherosclerosis.
 ...
PMID:The role of the stress-related anti-inflammatory hormones ACTH and cortisol in atherosclerosis. 1948 4