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)

In a previous study we observed that calcitonin increases beta-endorphin, ACTH, and cortisol secretion. We assumed that calcitonin might have a modulatory role on the pituitary function. The present study was initiated to clarify whether this effect is due to a direct pituitary stimulation or to an indirect stimulation through CRF (corticotropin releasing factor). Fourteen healthy subjects, aged 30-60 years were investigated. All the subjects received 100 IU Salmon calcitonin Sandoz i.v. at 8 a.m. (time 0). Plasma beta-endorphin, ACTH and cortisol were estimated every 30 min from -30 to 120 min by specific radioimmunoassay. The same parameters were estimated a second time, at the same intervals, when cyproheptadine 8 mg (7 subjects) and 40 mg propranolol (7 subjects) were given per os at -30 min and calcitonin i.v. at time 0. beta-endorphin, ACTH and cortisol levels (Mean +/- SEM) rose significantly after calcitonin (peak value at 30-90 min) from 5.2 +/- 0.7 to 15.1 +/- 2.6 pmol/l; from 43.0 +/- 2.7 to 70.7 +/- 4.1 pg/ml and from 10.6 +/- 1.5 to 19.6 +/- 2.1 micrograms/100 ml respectively (p less than 0.0001 by analysis of variance and covariance and repeated measures). Propranolol 40 mg (per os) administered at time -30 did not alter the response of beta-endorphin, ACTH and cortisol to calcitonin (infused at time 0). Cyproheptadine, the antiserotonergic substance that inhibits the synthesis and release of CRF completely inhibited the stimulatory effect of calcitonin. We conclude that probably calcitonin has a modulatory role on the hypothalamo-pituitary adrenal axis and that it acts at the hypothalamic level probably by stimulating CRF secretion.
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PMID:Antiserotonergic inhibition of calcitonin-induced increase of beta-endorphin, ACTH, and cortisol secretion. 285 Mar 48

Synthetic bovine parathyroid hormone containing the 1-34 NH2 terminal amino acids [bPTH-(1-34)] is capable of inhibiting stimulated uterine contraction. The purpose of the present investigation is to determine whether the inhibitory action of bPTH-(1-34) is a direct action of the hormone fragment. The effect of different synthetic preparations of bPTH-(1-34), salmon calcitonin, corticotropin-inhibiting peptide and bovine serum albumin on oxytocin-stimulated uterine contraction was determined. In addition, the effects of atropine, propranolol, phentolamine, pyrilamine, cimetidine and the prostaglandin synthetase inhibitor indomethacin on the inhibitory action of bPTH-(1-34) on uterine contraction was determined. Both synthetic preparations of bPTH-(1-34) inhibited oxytocin-initiated contractions similarly. Salmon calcitonin, corticotropin-inhibiting peptide, and bovine serum albumin did not alter oxytocin-stimulated uterine contractions. The salmon calcitonin also did not alter the ability of bPTH-(1-34) to exert its inhibitory effect on uterine contraction. Cholinergic, alpha and beta adrenergic, histaminergic (H1 and H2) and prostaglandin synthetase inhibitors did not alter the action of bPTH-(1-34). These results suggest that the action of bPTH-(1-34) is 1) not due to the presence of a contaminant in the synthetic hormone preparation and 2) that the effect could be due to a direct action effect of the hormone fragment on uterine tissue.
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PMID:Direct effect of parathyroid hormone on rat uterine contraction. 608 71