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)

The effect of 90-min heat exposure (46 degrees C, 35 mbar) on plasma aldosterone (PA) patterns was studied and the respective roles of plasma renin activity (PRA), adrenocorticotropin (ACTH), Na+ and K+ concentrations in the control of PA response were in investigated in eight subjects on a low sodium diet and in five subjects on a high sodium diet. In all subjects, transitory PA increases of varying importance were observed, which were not related to sweat losses (less than 1% bodyweight) or to rectal temperature rise. In sodium-repleted subjects, basal PA and PRA levels as well as heat-induced rises were low (mean PA peak level = 12.62 +/- 1.15 ng/100 ml). They were enhanced by sodium depletion and PA reached a mean peak level of 34.07 +/- 2.73 ng/100 ml. But, in both conditions, the heat-induced PA peaks were 3-times higher than the initial levels. PA correlated with PRA in all but one of the sodium-repleted subjects and in 6 of the 8 sodium-depleted subjects. ACTH release, as measured by plasma cortisol (PC) levels, occurred in those subjects who noted an increased feeling of annoyance and discomfort. Thus, PA correlated positively with PC in 4 sodium-depleted subjects. A high sodium intake improved heat-tolerance. Plasma K+ and Na+ concentrations were not significantly modified by exposure to heat. PA increases can occur without concomitant changes in PRA, PC, K+ or Na+, which suggests that an additional factor may play a role in aldosterone regulation during acute heat exposure.
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PMID:Plasma aldosterone, renin activity, and cortisol responses to heat exposure in sodium depleted and repeleted subjects. 44 70

Experiments were conducted to determine if endogenously produced beta-endorphin and met-enkephalin exert a physiological inhibition on luteinizing hormone-releasing hormone (LHRH) release in the central nervous system of sheep. Twenty-two mature ewes were implanted with unilateral guide tubes, through which matched infusion cannulae could be inserted without discomfort once daily for intracerebral (i.c.) infusion of three anti-opioid treatments: naloxone (50 micrograms in 20 microliters), sheep antisheep beta-endorphin (ABE; 20 microliters of 1:25) or sheep anti-met-enkephalin (AME; 20 microliters of 1:25) and of two control treatments: nonimmune sheep serum (20 microliters of 1:25) or sheep antiporcine thyroglobulin (20 microliters of 1:25). To detect abrupt disinhibition of LHRH release by anti-opioid treatments, serum luteinizing hormone (LH) was quantified at 10-min intervals for 1-2 h before and after each i.c. infusion. Complete trials consisted of 3-4 different anti-opioid or control i.c. infusions once daily at a single site over a period of 2-3 days during the luteal phase of recurring estrous cycles. Results were statistically evaluated within each ewe since complete trials were replicated 2-5 times within each ewe and because no 2 ewes could have i.c. infusions in identical locations. Anatomical generalizations were possible when LH responses to anti-opioid treatments were similar for several ewes with i.c. infusion sites in comparable brain regions. However, it was not possible to make such generalizations when infusion sites were not comparable in other ewes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intracerebral immunoneutralization of beta-endorphin and met-enkephalin disinhibits release of pituitary luteinizing hormone in sheep. 212 63

Discovery of the endogenous opiate system of the brain has revolutionized the study of pain and pain management. In this study a convenience sample of 10 pregnant women, 16 nonpregnant women, and 18 men were studied to determine if changes in plasma beta-endorphin-like immunoreactivity affected pain perception during labor. Pregnant women had plasma levels of beta-endorphin significantly higher than nonpregnant women at the midpoint of their menstrual cycle, t = 3.74, df = 31, p = .007. Self-reported pain perception scores were not correlated with plasma beta-endorphin levels. However, as labor progressed, the women reported increased discomfort between contractions and during contractions while beta-endorphin levels increased only slightly. Close examination of the pain pattern indicates that pain perceived by the women between contractions increased at a greater rate than during contractions. This pattern suggests that opiate-active beta-endorphin may increase the ability of women to tolerate acute pain.
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PMID:Beta-endorphin levels during pregnancy and labor: a role in pain modulation? 252 22

Sensibility threshold, mental health, and plasma beta-endorphin, cortisol, and prolactin levels were studied in 15 patients suffering from chronic orofacial pain or discomfort, six of them with oral lichen planus and nine with atypical facial pain. Five patients were used as controls. The results showed a difference in mental health and sensibility threshold; the mentally more disturbed had a lower sensibility threshold. The patients suffering from chronic pain were more frequently mentally disturbed than the patients in the control group and also had a lower sensibility threshold than the controls. Neither severity of pain nor mental disturbance correlated with the endocrine markers.
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PMID:Sensibility threshold, mental health, and endocrine markers in patients with chronic orofacial pain. 259 84

Eight healthy young men were studied during three periods of heat exposure in a Finnish sauna bath: at 80 degrees C dry bulb (80 D) and 100 degrees C dry bulb (100 D) temperatures until subjective discomfort, and in 80 degrees C dry heat, becoming humid (80 DH) until subjective exhaustion. Oral temperature increased 1.1 degrees C at 80 D, 1.9 degrees C at 100 D and 3.2 degrees C at 80 DH. Heart rate increased about 60% at 80 D, 90% at 100 D and 130% at 80 DH. Plasma noradrenaline increased about 100% at 80 D, 160% at 100 D and 310% at 80 DH. Adrenaline did not change. Plasma prolactin increased 2-fold at 80 D, 7-fold at 100 D and 10-fold at 80 DH. Blood concentrations of the beta-endorphin immunoreactivity at 100 D, adrenocorticotropic hormone (ACTH) at 100 D and 80 DH, growth hormone at 100 D and testosterone at 80 DH also increased, but cortisol at 80 D and 100 D decreased. The plasma prostaglandin E2 and serum thromboxane B2 levels did not change. Patterns related to heat exposure were observed for heart rate, plasma noradrenaline, ACTH and prolactin in the three study periods.
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PMID:Haemodynamic and hormonal responses to heat exposure in a Finnish sauna bath. 275 81

Plasma beta-endorphin (beta-EP), beta-lipotropin (beta-LPH), and cortisol concentrations were measured by perimenstrual period in 11 patients affected by premenstrual syndrome (PMS) and in 8 asymptomatic healthy volunteers. Blood samples were collected every 2 to 3 days, for 1 month, starting from midcycle. The Menstrual Distress Questionnaire (MDQ) was administered during the testing period. Plasma beta-LPH and cortisol levels remain stable during the perimenstrual period, in both controls and PMS patients. On the contrary, PMS patients showed a decrease of plasma beta-EP in the week preceding menses and during the first days of menstrual flow. Beta-EP values of PMS patients regain normal levels during the next follicular phase. No changes of beta-EP levels were recorded in asymptomatic women. MDQ scores revealed that PMS patients complained of water retention, pain discomfort, and mood swings. The transient and reversible decrease of plasma beta-EP in PMS patients near to and at menses remains to be clarified.
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PMID:Premenstrual fall of plasma beta-endorphin in patients with premenstrual syndrome. 295 25

Relief of discomfort during acute myocardial ischemia is usually accomplished with a narcotic analgesic. Because these medications may cause unpleasant symptoms and exert a possibly adverse hemodynamic effect, the availability of alternative analgesic medication would be advantageous. Nitrous oxide is a commonly used potent analgesic gas. Nitrous oxide has been used to relieve ischemic discomfort during myocardial infarction. The current study was undertaken to corroborate that data in a randomized, blinded, cross-over study and to begin to explore a mechanism for the analgesic effect. Twelve patients with typical ischemic chest discomfort and a suspected myocardial infarction were included in the study. Each patient received a 30-minute inhalation treatment of 30% nitrous oxide/70% oxygen and 30 minutes of 30% room air/70% oxygen. Patients were blinded to their treatment and were randomized to receive nitrous oxide first, then room air, or vice versa. A semiquantitative assessment of the severity of chest discomfort was made before, during, and at the conclusion of each treatment together with a measurement of plasma beta-endorphin levels using a venous blood sample. Eleven of the 12 patients reported a significant reduction in the intensity of their chest discomfort during the nitrous oxide inhalation, but none had pain relief during the control period. Beta-endorphin levels fell to a greater extent during the inhalation of nitrous oxide than during the control period (51% versus 26%; P less than .05). No significant adverse effects were noted and most patients slept during the nitrous oxide inhalation. It is concluded that nitrous oxide anesthesia is a superior method of pain relief in patients with ischemic heart disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nitrous oxide anesthesia in patients with ischemic chest discomfort: effect on beta-endorphins. 296 38

The sauna induces changes in the secretion of hormones, some similar to changes induced in any other stress situation and others characteristic of exposure to the sauna. Noradrenaline is usually the only catecholamine raised by the sauna in people accustomed to it. The secretion of the antidiuretic hormone is increased and the renin-angiotensin-aldosterone system is activated. The concentrations of the growth hormone and prolactin, in particular, secreted from the anterior pituitary are increased in the circulation. The concentration of the immunoreactive beta-endorphin in blood may also increase which may reflect the feeling of pleasure or, on the other hand, discomfort induced by the sauna. The views on the effects of the sauna on the secretion of the ACTH and cortisol are partly contradictory, probably due to differing ways of taking the sauna bath. In Finnish sauna takers the concentration of cortisol in blood is not usually increased. The changes induced by the sauna in various hormone concentrations in the circulation are, however, normalized within a couple of hours after the heat stress.
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PMID:How the sauna affects the endocrine system. 321 98

For patients who require treatment over a period of some years, intranasal administration of synthetic salmon calcitonin (SSCT) obviates the discomfort associated with administration by injection. Moreover, this mode of administration is not associated with the side effects normally encountered when calcitonin is injected intramuscularly or subcutaneously. The aim of this study was to assess, in normal subjects, the biological activity of nasal SSCT by comparing the fluctuations of parameters reflecting calcium-phosphorus metabolism after nasal instillation, injection of SSCT and injection of placebo, respectively. In nine healthy subjects, this instillation of 200 IU of SSCT into the nasal cavity caused a fall in serum calcium, a fall in serum phosphorus and a transient rise in parathyroid hormone levels similar to that observed after the intramuscular (i.m.) injection of 80 IU of SSCT. SSCT whether administered by the nasal route or by injection, does not inhibit endogenous calcitonin secretion. There were no changes in serum beta-endorphin, magnesium or erythrocyte magnesium levels after administration of calcitonin by the intranasal route or by injection.
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PMID:Assessment of the biological effectiveness of nasal synthetic salmon calcitonin (SSCT) by comparison with intramuscular (i.m.) or placebo injection in normal subjects. 350 25

In an attempt to locate biochemical markers specific for fetal distress we measured the amniotic concentrations of beta-endorphin, ACTH, cortisol, dopamine, norepinephrine and epinephrine with its major metabolite metanephrine (MN) in pregnancies with documented fetal well-being and pregnancies complicated by hypertension and fetal distress. While higher levels of cortisol and MN were found only in a selected subgroup of highly compromised subjects (p < 0.001 and p < 0.005, respectively), beta-endorphin increased significantly under conditions of moderate or severe intrauterine sufferance (p < 0.001 in both cases). Due to higher levels of the opioid even during the initial stage of fetal discomfort we evaluated its characteristics as a possible clinical marker. Specificity was 88.5%, whereas the sensitivity of 65.6% in the moderately compromised subgroup increased to 88.9% in severely suffering fetuses. Although more accurate and mainly real-time information on the fetal health status is obtained by means of biophysical methods, the determination of amniotic fluid beta-endorphin might be of clinical usefulness in prenatal diagnosis.
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PMID:Stress mediators in the amniotic compartment in relation to the degree of fetal distress. 781 78


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