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 reaction of the oxygen isotope exchange (18O-exchange) was studied in the course of the Na, K-ATPase reaction. It was shown that the intermediary and direct 18O-exchanges occurred in the system in the presence of both ATP and p-NPP. These findings are indicative of the same intermediate during the hydrolytic process in both cases. The intermediary 18O-exchange was activated by N-ethylmaleimide, hydroxylamine and 2.0--1.5 18O atoms, respectively. The detection of 18O-exchange Ouabain had no effect on the exchange. The levels of intermediary 18O-exchange during ATP and p-NPP hydrolyses were equal to 1.3--1.4 and 2.0--1.5 18O atoms, respectively. The detection of 18O-exchange reactions at the intermediary steps of both ATP and p-NPP hydrolyses implies the identity of certain stages in the destruction of these substrates by Na, K-ATPase.
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PMID:[18 O-exchange during ATP and n-nitrophenylphosphate hydrolysis by Na, K-ATPase from bovine brain]. 14 48

The effect of bradykinin (BK) on the release of beta-endorphin-like immunoreactivity (beta-END-LI) in rats was studied in in vivo and in vitro. Intraperitoneal injection of BK at 5 micrograms/100 g body weight resulted in a significant increase in the plasma beta-END-LI level after 15 min. BK at concentrations of 10(-12)-10(-7) M also caused dose-dependent stimulation of beta-END-LI release from the dispersed cells of the anterior pituitary of rats. On gel chromatography, the beta-END-LI released by incubation of the cells with 10(-7) M BK separated into two components; one eluted in the same positions as human beta-lipotropin and the other as human beta-endorphin. BK did not stimulate beta-END-LI release in Ca++-free medium. Addition of 10(-3) M verapamil, 10(-6) M dexamethasone or 10(-7) M somatostatin to the incubation medium inhibited BK-induced beta-END-LI release from the cells. Ouabain (10(-5) M) also stimulated beta-END-LI release, but its effect was not additive with that of BK. These results indicate that BK stimulates beta-END-LI release and that calcium ion is involved in the mechanism of this effect.
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PMID:[In vivo and in vitro effects of bradykinin on the release of beta-endorphin-like immunoreactivity]. 286 30

Repetitive preganglionic nerve stimulation increases cyclic guanosine 3':5'-monophosphate (cGMP) content in rat superior cervical ganglia by a mechanism requiring Ca++ but resistant to blockade by cholinergic receptor antagonists. Similarly, 45Ca-uptake during prolonged preganglionic nerve stimulation is unaffected by hexamethonium or atropine. These findings indicate that nerve stimulation increases cGMP accumulation and 45Ca-uptake by a noncholinergic mechanism Substance P, met-enkephalin and luteinizing hormone-releasing factor have little or no effect on cGMP content. By contrast, bethanechol causes a 3-fold increase in cGMP content and postganglionic cell firing. Thus, as reported by others, muscarinic receptor activation increases ganglionic cGMP[. 4-Aminopyridine causes an increase in cGMP of resting ganglia that requires Ca++ and the nerve terminal is blocked by tetrodotoxin but unaffected by atropine or hexamethonium. Ouabain also increases ganglionic cGMP content by a process that requires Ca++ and the nerve terminals. Like preganglionic nerve stimulation, 4-aminopyridine and ouabain cause cGMP accumulation in the nerve terminals or in the ganglion cells as a consequence of releasing a noncholinergic transmitter. The uptake of Ca++ by ganglion cells is not an adequate stimulus for cGMP accumulation because the nicotinic receptor agonist dimethylphenylpiperazinium increases 45Ca-uptake but has no effect on cGMP formation in ganglia.
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PMID:Cyclic guanosine 3':5'-monophosphate accumulation and 45Ca-uptake by rat superior cervical ganglia during preganglionic stimulation. 611 99

The effect of substance P (SP) on the release of beta-endorphin-like immunoreactivity (beta-EpLI) in rats was studied in vivo and in vitro. Intravenous injection of 5 micrograms/100 g BW of SP resulted in significant increase in the plasma beta-EpLI level after 15 and 30 min. SP at concentrations of 10(-9) to 10(-6) M also caused dose-dependent stimulation of beta-EpLI release from dispersed cells of rat anterior pituitary. On gel-chromatography, the beta-EpLI released by incubation of the cells with 10(-7) M SP separated into two components, eluted in the same positions as human beta-lipotropin and human beta-Ep, respectively. Release of beta-EpLI from the cells was increased by the addition of K+ at high concentration (53 mM) in a Ca++-dependent manner. Addition of 10(-3) M verapamil to the incubation medium inhibited SP-induced beta-EpLI release from the cells. Ouabain (10(-5) M) had a stimulatory effect on beta-EpLI release which was not additive with that of SP. These results indicate that SP acts directly on the anterior pituitary cells to stimulate beta-EpLI release and that calcium ion is involved in the mechanism of this effect.
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PMID:In vivo and in vitro effects of substance P on the release of beta-endorphin-like immunoreactivity. 618 1

The effect of cholecystokinin octapeptide (CCK-8) on the release of beta-endorphin-like immunoreactivity (beta-EpLI) in rats was studied in vivo and in vitro. Intravenous injection of 5 micrograms/100 g body weight of CCK-8 resulted in significant increase in the plasma beta-EpLI level after 10 and 20 min. CCK-8 at concentrations of 10(-10) - 10(-6) M also caused dose-dependent stimulation of beta-EpLI release from dispersed cells of rat anterior pituitary. However, CCK-4 and desulfated CCK-8 had no effect. On gel chromatography, the beta-EpLI released by incubation of the cells with 10(-8) M CCK-8 separated into two components, eluted in the same positions as human beta-lipotropin and human beta-endorphin, respectively. CCK-8 did not stimulate beta-EpLI release in Ca++-free medium. A 23187 at concentrations of 10(-6) - 10(-3) M caused dose-dependent stimulation of beta-EpLI release from the cells. Addition of 2 X 10(-3) M CoCl2, 10(-3) M verapamil or 10(-7) M dexamethasone to the incubation medium inhibited CCK-8-induced beta-EpLI release from the cells. Dibutyryl cyclic GMP (3 X 10(-3) M) inhibited CCK-8-induced beta-EpLI release from the cells. Ouabain (10(-5) M) also stimulated beta-EpLI release but its effect was not additive with that of CCK-8. These results indicate that CCK-8 acts directly and specifically on anterior pituitary cells to stimulate beta-EpLI release and that calcium ion is involved in the mechanism of this effect.
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PMID:In vivo and in vitro effects of cholecystokinin octapeptide on the release of beta-endorphin-like immunoreactivity. 630 91

We studied the role of sodium ions in mediating basal and stimulated ACTH release from perifused rat anterior pituitary cells by exposing the cells to the sodium channel opener veratridine or the Na+/K(+)-adenosine triphosphatase inhibitor ouabain to increase the intracellular Na+ concentration or, conversely, by omitting Na+ from the perifusion medium or blocking Na+ entry into the cell with tetrodotoxin, a voltage-dependent sodium channel blocker, to decrease the intracellular Na+ concentration. Neither tetrodotoxin nor Na(+)-free medium had a significant effect on 100 nM arginine vasopressin (AVP) or 10 nM ovine corticotropin-releasing hormone (CRH)-induced ACTH secretion. Veratridine increased basal ACTH secretion by 122% (41.3 +/- 2.9 vs. 18.6 +/- 0.4 pg/min; P < 0.001), the initial spike phase of the response to AVP by 65% (0.28 +/- 0.01 vs. 0.17 +/- 0.03 ng/3 min; P < 0.005), the subsequent sustained phase to AVP by 129% (0.16 +/- 0.01 vs. 0.07 +/- 0.01 ng/7 min; P < 0.005), and the total response to CRH by 70% (0.39 +/- 0.01 vs. 0.23 +/- 0.04 ng/10 min; P < 0.05). Ouabain increased basal ACTH secretion by 39% (45.7 +/- 2.8 vs. 32.9 +/- 2.1 pg/min; P < 0.05), the initial spike phase of the response to AVP by 88% (0.32 +/- 0.02 vs. 0.17 +/- 0.01 ng/3 min; P < 0.005), the sustained phase response to AVP by 67% (0.10 +/- 0.01 vs. 0.06 +/- 0.01 ng/7 min; P < 0.05), and the total integrated response to CRH by 49% (0.88 +/- 0.09 vs. 0.59 +/- 0.03 ng/10 min; P < 0.05). However, the effects of both veratridine and ouabain on basal ACTH secretion were significantly attenuated in Ca(2+)-free EGTA-containing medium, suggesting that this effect was indirect, due to membrane depolarization and consequent influx of extracellular Ca2+. Dexamethasone (100 nM) had no effect on the ACTH response to either veratridine or ouabain. We conclude that changes in the intracellular Na+ concentration and sodium channel activity are not directly involved in AVP- or CRH-induced ACTH secretion.
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PMID:The role of sodium in mediating adrenocorticotropin secretion by perifused rat anterior pituitary cells. 778 18

1. Ouabain or a related stereoisomer, termed endogenous ouabain, has been identified in adrenal cortex tissue and culture medium from adrenocortical cells. 2. Angiotensin II and adrenocorticotropin, the main activators of aldosterone secretion from adrenal glomerulosa cells appear to increase the production of this compound. 3. The purpose of this review is to briefly discuss recent available experimental evidence suggesting that endogenous ouabain is secreted by the zona glomerulosa of the adrenal gland.
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PMID:Is ouabain produced by the adrenal gland? 979 6

Digoxin, a cardiac glycoside, is used to increase cardiac contractility via inhibition of Na(+)/K(+)-adenosinetriphosphatase (ATPase) and increase intracellular calcium in congestive heart failure. Inhibitory effects of digoxin have been demonstrated on the biosynthesis of gonadal hormones and adrenal glucocorticoids in rats. However, acute effects of digoxin on levels of adrenal corticosteroid hormones in the primates in vivo are uncertain. Therefore, we test the hypothesis that a single injection of digoxin decreases the secretion of aldosterone and cortisol in monkeys. An intravenous injection of digoxin (1 microg/kg) inhibited basal and adrenocorticotropin (ACTH)- or KCl-stimulated aldosterone release in monkeys. Furthermore, digoxin induced a decrease in ACTH- and KCl-stimulated cortisol release. Administration of digoxin did not alter plasma concentrations of Na(+) and K(+). Ouabain, a selective inhibitor of Na(+)/K(+)-ATPase, did not affect ACTH- or KCl-stimulated aldosterone and cortisol release. These results revealed that injection of digoxin induced an inhibitory effect on aldosterone and cortisol secretion in monkeys. Because ouabain did not affect levels of plasma aldosterone or cortisol, we suggest that (1) the Na(+)/K(+)-ATPase pathway may not be involved in the mechanism of action of digoxin on aldosterone or cortisol secretion in monkeys and/or (2) the Na(+)/K(+)-ATPase is more sensitive to digoxin than to ouabain in monkeys.
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PMID:Acute effects of digoxin on plasma aldosterone and cortisol in monkeys. 1905 31