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)

Some recent studies suggest that changes in the endogenous opioid peptides (POE) secretion during stress may be involved in various hemodynamic, respiratory and hormonal responses to exercise. To evaluate the relationship between fitness and POE release, 10 mixed-type exercise trained athletes (A) and 10 sedentary normal controls (C) were examined by bicycle stress testing; maximum oxygen uptake (VO2max) and peak work load (PWL) were greater in A than C (VO2max = 61.8 +/- 5.2 vs 40.2 +/- 6.1 ml/kg; PWL = 1525 +/- 229 vs 915 +/- 305 kgm.both p less than 0.01). After 24 hours A and C underwent rectangular bicycle stress testing (two 20' steps at 60% and 80% VO2max). Total plasmatic beta-endorphin (BEP) and its precursor beta-lipotropin (BLPH) were dosed by radioimmunoassay at rest, at 60% VO2max, at 80% VO2max and after complete recovery. Physical exercise caused a transient rise of BEP + BLPH plasma levels in both A and C. In A the increase was greater and occurred earlier than in C. The POE release under submaximal exercise showed a close correlation with oxygen uptake and therefore with fitness. This relation appeared in A at both low and high effort levels, whereas in C it was more strict at higher effort level. There results suggest that POE system play an important role in the adaptive mechanisms in sport practice.
G Ital Cardiol 1987 Oct
PMID:[Release of beta-endorphin and beta-lipotropin during submaximal exertion in sedentary and active subjects. Endogenous opiate peptides during exertion in sedentary and active subjects]. 296 79

To verify whether beta-endorphin plasma levels influence the presence of anginal symptoms, 74 consecutive male patients were studied. All patients had previously documented coronary artery disease and reproducible exercise-induced myocardial ischemia. Thirty-five patients (Group I) had a history of angina and reported anginal symptoms during exercise stress testing; 39 patients (Group II) were asymptomatic and had documented silent myocardial ischemia during exercise. Baseline beta-endorphin plasma levels were measured in blood samples taken before exercise stress testing and analyzed by beta-endorphin-I125-RIA Kit-NEN (a radioimmunoassay method). The mean baseline beta-endorphin plasma level was 22.5 +/- 19 pg/ml in patients with anginal symptoms compared with 43.7 +/- 28 pg/ml in asymptomatic patients (p less than 0.001). Baseline blood pressure and heart rate-systolic pressure (rate-pressure) product at baseline and at ischemia threshold (1 mm ST segment depression) were similar in the two groups. Group II patients had a longer exercise duration (p less than 0.01), more pronounced ST segment depression (p less than 0.001) and a higher peak rate-pressure product (p less than 0.01). The extent of coronary artery disease, ejection fraction and left ventricular end-diastolic pressure were similar in the two groups. These data suggest that higher baseline beta-endorphin plasma levels may play a role in the decreased sensitivity to pain in patients with silent myocardial ischemia. In addition, different beta-endorphin levels can be associated with a different sensitivity to pain.
J Am Coll Cardiol 1988 Apr
PMID:Correlation between beta-endorphin plasma levels and anginal symptoms in patients with coronary artery disease. 296 73

Although silent myocardial ischemia is a well recognized phenomenon, the reasons for the lack of symptoms in patients with coronary artery disease (CAD) is unclear. Because the endogenous opioid beta-endorphin has been related to pain modulation, plasma beta-endorphin levels were studied before, during and after exercise-induced ischemia in symptomatic and asymptomatic men. Because beta-endorphin responses have been closely linked to adrenocorticotropic hormone (ACTH) and cortisol responses, these hormones also were measured. Nine symptomatic and 12 asymptomatic patients with a high probability (at least 95%) of CAD and 8 apparently healthy men completed a Bruce protocol treadmill test. Blood samples were drawn before, during and 10 minutes after exercise. During exercise the measured hormones showed no significant increases from basal levels. However, plasma beta-endorphin, ACTH and cortisol levels were significantly elevated (p less than or equal to 0.01) 10 minutes after exercise in all 3 groups. There was no significant difference in plasma beta-endorphin levels during or after exercise between the symptomatic and asymptomatic patients with CAD. Thus, differences in circulating levels of beta-endorphin, ACTH and cortisol are not associated with the presence or absence of pain during exercise-induced myocardial ischemia.
Am J Cardiol 1987 Apr 01
PMID:Plasma beta-endorphin levels in silent myocardial ischemia induced by exercise. 303 88

Plasma beta-endorphin levels were measured by radioimmunoassay before and after exercise in 25 patients with coronary artery disease. Eighteen patients were men and 7 were women; age range was 36 to 75 years (mean 60). All patients had angina pectoris, a positive treadmill test response or positive exercise radionuclide findings. The mean preexercise plasma endorphin level was 4.9 +/- 3.0 pmol/liter (range 0.7 to 13.5). The mean postexercise plasma endorphin level of 6.6 +/- 4.6 mol/liter (range 0 to 19.5) was significantly higher (p less than 0.05). A significant positive correlation was seen between postexercise endorphin levels and time to onset of angina (r = 0.4, p = 0.03). There were negative correlations between postexercise endorphin levels and occurrence (r = -0.4, p = 0.04) and duration of angina (r = -0.4, p = 0.05). No association was found for maximal heart rate-blood pressure product, workload, time to ST-segment depression or stress ejection fraction. A positive correlation was found between rest left ventricular ejection fraction and postexercise endorphin levels (r = 0.5, p = 0.02). In conclusion, in patients with exercise-induced myocardial ischemia, plasma beta-endorphin levels are increased after exercise; postexercise endorphin levels are related to timing and occurrence (presence or absence) of angina; and endorphins may alter the perception of pain caused by myocardial ischemia.
Am J Cardiol 1987 Mar 01
PMID:Endorphins are related to pain perception in coronary artery disease. 382 89

The effects of adrenocorticotropic hormone (ACTH) on systolic blood pressure, and echocardiographic indexes of heart size and function were investigated in 14 infants. After 25 days (range 13 to 46) of treatment with ACTH, systolic blood pressure increased from 93 +/- 9 to 118 +/- 20 mm Hg (p < 0.001; mean +/- 1 SD). Systolic hypertension (systolic blood pressure greater than the 95th percentile for age) developed in 10 of 14 infants and was associated with an increase in left ventricular (LV) shortening fraction from 41 +/- 5% to 52 +/- 8% (p < 0.001). Myocardial hypertrophy and an increase in echocardiographic indexes of myocardial contractility were observed also. To assess the temporal relation between the onset of systolic hypertension and these cardiac changes, data from 8 infants with serial echocardiograms and blood pressure determinations were examined. After a mean 14 days (range 8 to 18) of ACTH, LV shortening fraction increased from 39 +/- 6% to 53 +/- 8% (p < 0.01), whereas systolic blood pressure remained normal in 7 of 8 infants. In addition, a decrease in LV end-systolic dimension was observed during this early phase. This report documents myocardial changes in individual patients, which occur before and during the development of systolic hypertension.
Am J Cardiol 1994 Jan 01
PMID:Cardiac size and function during adrenocorticotropic hormone-induced systolic systemic hypertension in infants. 827 78

The differences between diabetic and nondiabetic patients with silent myocardial ischemia were investigated. Based on the results of previous exercise testing, a total of 110 patients (15 diabetic and 95 nondiabetic) with exercise-induced myocardial ischemia were divided into the following 3 groups: 15 diabetics with silent myocardial ischemia, 49 nondiabetics with silent myocardial ischemia, and 46 nondiabetics with anginal symptoms. All patients underwent treadmill exercise testing and 24-hour ambulatory electrocardiographic recording. Before and during exercise, blood samples from the antecubital vein were obtained to determine the plasma beta-endorphin levels, and the pain threshold of each patient was measured with the electrical skin stimulation test. Furthermore, with regard to the ambulatory electrocardiographic recording, the mean of the SDs of all normal sinus RR intervals during successive 5-minute recording periods over 24 hours was analyzed and considered as an index of the autonomic function. The plasma beta-endorphin level during exercise was significantly greater in nondiabetic patients with silent ischemia than in diabetic ones. The SD mean was significantly less in the diabetic group than in the 2 nondiabetic ones. The findings suggest that the role of beta endorphin in diabetic patients with silent myocardial ischemia may be less significant than in nondiabetic ones; therefore, a diabetic neuropathy that affects the autonomic pain fibers that innervate the heart may be involved in the mechanism of silent myocardial ischemia in diabetics.
Am J Cardiol 1993 Jul 15
PMID:Usefulness of plasma beta-endorphin level, pain threshold and autonomic function in assessing silent myocardial ischemia in patients with and without diabetes mellitus. 832 73

Circadian effects on PTZ-induced seizure thresholds alone and following drug pretreatment were studied in 720 male rats, divided into 40 groups of 18 each. Each rat was tested only once, at one of eight clock hours and under one of five drug pretreatments. Clear cyclic changes in thresholds were found. Drug effects on the rhythm were similar for DSIP and beta-endorphin, which produced higher thresholds during the night periods, while d-amphetamine and melatonin decreased the threshold during that period. All drugs increased the vulnerability to seizures relative to the saline control during the daytime, while only beta-endorphin and DSIP offered improved protection during the night hours. The possibility of dopaminergic mediation is suggested to account for the effects.
 ...
PMID:Circadian effects of beta-endorphin, melatonin, DSIP, and amphetamine on pentylenetetrazol-induced seizures. 848 98

In order to investigate the changes of endogenous opiate systems in hypertension and their possible role in the pathogenesis in hypertension, we measured plasma concentrations of beta-endorphin, leucine-enkephalin, neurotension, arginine vasopressin, plasma renin activity and angiotensin II by radioimmunoassay in 60 normal persons and 120 patients with essential hypertension. The results showed that the patient group had lower levels of beta-endorphin and leucine enkephalin (P < 0.001), higher levels of arginine vasopressin, plasma renin activity and angiotensin II (P < 0.01, P < 0.05 and P < 0.05, respectively), and normal level of neurotensin, as compared with those in normal group. Plasma levels of leucine-enkephalin was correlated negatively to the mean artery pressure (r = -0.196, P < 0.05). Plasma level of arginine vasopressin was correlated to the duration of the hypertension (r = 0.216, P < 0.05). After 150 min and 14 days of treatment with clonidine, plasma levels of beta-endorphin, leucine-enkephalin increased significantly (< 0.01) and correlated negatively with the decrease of the mean artery pressure (r = -0.340 and r = -0.436 at 150 min, r = -0.369 and r = -0.441 on the 14th day, respectively, P < 0.01). Plasma renin activity and angiotensin II decreased significantly (P < 0.05 and P < 0.01). Arginine vasopressin and neurotensin did not change significantly. After intravenous administration of opiate antagonist-naloxone, the blood pressure and heart rate increased significantly (P < 0.01). The results suggested that the changes of endogenous opioids may be involved in the pathogenesis of hypertension and in the antihypertensive action of clonidine.
Int J Cardiol 1995 Oct
PMID:Plasma levels of beta-endorphin, leucine enkephalin and arginine vasopressin in patients with essential hypertension and the effects of clonidine. 858 72

Cardiopulmonary bypass (CPB) results in a diffuse inflammatory response characterized in part by hyperstimulation of leukocytes. We have previously shown that this hyperstimulation appears to be due, in part, to an increase in the release of biological response modifiers (BRMs) such as cytokines. In the present study, we evaluated the ability of a naturally occurring immunocyte inhibitory substance, alpha-melanocyte-stimulating hormone (alpha-MSH), to prevent the hyperstimulation caused by CPB. Monocytes and granulocytes were pretreated with alpha-MSH (10(-6) M) before exposing the cells to plasma obtained from patients who had undergone CPB, as CPB plasma would stimulate native monocytes and granulocytes in a manner similar to that observed in CPB patients. Pretreatment of these cells with alpha-MSH significantly diminished the hyperstimulation induced by CPB plasma in a concentration-dependent manner. In contrast, when the cells were first or simultaneously exposed to CPB plasma and then to alpha-MSH, alpha-MSH had no effect. Furthermore, use of the specific neutral endopeptidase inhibitor, phosphoramidon, significantly increased the efficacy of alpha-MSH in inhibiting CPB-induced immunocyte activation. The data demonstrate that pretreatment of monocyte/macrophages and granulocytes with alpha-MSH effectively inhibits the immune hyperstimulation induced by CPB-plasma exposure. In addition, the data strongly suggest that preexposure to other naturally occurring immune inhibitory substances may diminish the hyperstimulation associated with CPB. The study also further confirms that this hyperstimulation may, in part, be due to BRMs released from immunocytes.
Int J Cardiol 1996 Apr 26
PMID:Hyperstimulation of leukocytes by plasma from cardiopulmonary bypass patients is diminished by alpha-MSH pretreatment. 879 93

The immunocyte behavior (conformational changes and locomotion in response to signal molecule challenge) in patients about to undergo elective cardiac surgery was studied to elucidate the effect of psychological anticipatory stress on the immune system. Granulocytes and monocytes from 10 patients and 35 non-surgical controls were examined. Computer-assisted microscopic image analysis, capable of measuring cellular conformational and velocity changes, was used to measure the responsiveness of these immunocytes to peptidergic and cytokine stimulation. Immunocyte desensitization would appear to account for the reduction in their abilities to respond to chemotaxic challenge associated with the pre-cardiac surgery state. Their abilities to respond to D-Ala2-Met-enkephalinamide (DAMA) were observed only at much higher concentrations than previously reported (10-11 M vs. 10-9 M prior to surgery). This finding, together with the observed decrease in adrenocorticotropin levels compared to non-surgical controls, suggests that neutral endopeptidase activity was elevated just prior to surgery. Indeed, neutral endopeptidase activity is statistically elevated in the pre-cardiac surgery state. Furthermore, glucocorticoid levels remained constant, within normal resting limits, in both groups. Thus, surgical anticipatory stress may manifest itself, in part, as a desensitization of various immunocytes. Thus, a psychological anticipatory stress response may be a precipitant of the desensitization. Although this desensitization seemed not to involve the entire hypothalamic-pituitary-adrenal axis, the data suggest that psychological anticipatory stress may initially involve and influence autoimmunoregulation.
Int J Cardiol 1996 Apr 26
PMID:Surgical anticipatory stress manifests itself in immunocyte desensitization: evidence for autoimmunoregulatory involvement. 879 95


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