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)

Microinjected directly into the preoptic anterior hypothalamus (POAH), beta-endorphin (0.74--7.4 nmol) induced an increase in rectal temperature (RT) in the free-moving rat. Whereas the initial phase of the endorphin-induced rise in RT was partially attenuated by naloxone (5 or 20 mg/kg i.p.) or naltrexone (3 mg/kg i.p.), the late phase was completely blocked by the prostaglandin synthetase inhibitor, indomethacin (15 mg/kg i.p.). Pretreatment with a combination of indomethacin and naloxone resulted in an almost total block of the endorphin-induced increase in RT. Furthermore, the central serotonin antagonist, methergoline (1 mg/kg i.p.) antagonized the endorphin-evoked fever indicating serotonin may mediate the rise in RT. In contrast to the fever evoked in the POAH, beta-endorphin (7.4 nmol), given into the lateral cerebral ventricle (LCV), elicited a marked drop in RT, catalepsy, and analgesia which were completely blocked by naloxone (5 mg/kg). Similar to morphine, beta-endorphin elicited a naloxone-reversible hyperthermia when administered into the subarachnoid space surrounding the spinal cord. The similarities between beta-endorphin and morphine in their actions on RT as well as the possible role of serotonin or prostaglandins in beta-endorphin's thermogenic action are discussed.
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PMID:Action of intracerebrally injected beta-endorphin on the rat's core temperature. 58 33

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

The vasopressin analogue, 1-desamino-8-arginine vasopressin (desmopressin), is a potent antidiuretic without the pressor effects of vasopressin. A total of 18 patients with acute renal colic due to stone disease received 40 microgramsf1p4mopressin intranasal spray with encouraging results. There was a significant decrease in the colic pain intensity from an initial mean visual analogue score of 67 +/- 17 mm. to 39 +/- 36 mm. within 30 minutes (p < 0.001). Eight patients (44.4%) had complete pain relief within 30 minutes of administering intranasal desmopressin spray. Nine of 10 patients who required intramuscular diclofenac sodium achieved complete pain relief within another 30 minutes. In other words, when intranasal desmopressin spray was administered before diclofenac sodium, 94.4% of the patients achieved complete pain relief and were discharged home. The mechanism of analgesic action of desmopressin in renal colic is uncertain. At the peripheral level, desmopressin may alleviate the acute renal colic through its potent antidiuretic effect or by relaxing the renal pelvic and ureteral smooth muscles. The central analgesic effect of desmopressin by stimulating the release of the hypothalamic beta-endorphin is proposed. We conclude that intranasal desmopressin spray can be used successfully in the treatment of renal colic. It may also replace prostaglandin synthetase inhibitors in treating renal colic with the advantage of avoiding the potential side effects. Further studies are needed to investigate whether the combination of desmopressin with analgesics or spasmolytic drugs offers competitive results compared with those achieved by prostaglandin synthetase inhibitors in the treatment of renal colic.
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PMID:Treatment of renal colic by desmopressin intranasal spray and diclofenac sodium. 771 52

Small volume intravenous infusions of hypertonic saline (HTS) increase blood pressure, heart rate, adrenocorticotropic hormone (ACTH), and cortisol by mechanisms that are not fully understood. We hypothesized that HTS infusions increase prostaglandin biosynthesis and that a prostaglandin synthase metabolite is responsible for mediating actions of HTS. We further hypothesized that thromboxane A2 (TxA2) is the specific metabolite responsible for mediating responses to HTS infusion. Adult female sheep (n=8) were chronically instrumented with vascular catheters and infused intravenously with 7.5% saline at a rate of 4 mL x kg(-1) over 5 min with or without pretreatment with the prostaglandin synthase inhibitor flunixin. Blood pressure, ACTH, and cortisol increased in response to HTS, and these responses were prevented by flunixin. Heart rate increased in response to HTS infusion, and flunixin reduced but did not prevent a heart rate response. Hematocrit decreased significantly in response to HTS but only following flunixin treatment. Arginine vasopressin increased but only modestly in response to HTS, and responses were not different following flunixin. Arterial pH, partial pressure of CO2, and partial pressure of O2 did not change. Circulating concentrations of thromboxane B2, a stable metabolite of TxA2 and an index of TxA2 formation, remained low and did not change in response to HTS. We conclude that heart rate, blood pressure, ACTH, and cortisol responses to HTS are mediated at least in part by a product of prostaglandin synthase metabolism. These responses were not due to increases in circulating concentrations of TxA2 but might involve local formation of TxA2 or some other prostaglandin synthase metabolite.
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PMID:Cardiovascular, adrenocorticotropin, and cortisol responses to hypertonic saline in euvolemic sheep are altered by prostaglandin synthase inhibition. 968 88