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)

Intravenous injection of nimodipine (1, 10 and 100 micrograms/Kg) raised plasma ACTH and beta-endorphin (beta-EP) level and reduced pituitary beta-EP content, in the rat. These effects were sharp and short-lasting. Nimodipine (10(-8), 10(-7), 10(-6) M) did not change basal and hypothalamic extract stimulated beta-EP release from pituitary tissue in vitro. Basal release of corticosterone from adrenal glands, superfused in vitro with the calcium antagonist (10(-7) - 10(-6) M), was not modified. However, ACTH-induced release was strongly reduced. Since glucocorticoids feedback regulates biosynthesis and cleavage of pro-opiocortin, nimodipine, which reduces adrenal gland responsiveness to ACTH, might reflexly increase beta-EP release from hypophysis.
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PMID:The calcium antagonist nimodipine increases beta-endorphin release from rat hypophysis through an action on adrenal glands. An "in vivo" and "in vitro" study. 609 28

The modulation of voltage-dependent calcium currents (I(Ca)) by corticotropin was studied in acutely dissociated rat amygdala neurons using whole-cell, patch-clamp recording techniques. Application of corticotropin(1-24) or corticotropin(4-10) increased I(Ca) in a concentration-dependent manner, with half-maximal effective concentrations of 65 and 176 nM and maximal increases of approximately 75% and approximately 50%, respectively. Nimodipine (1 microM) reduced the I(Ca) by approximately 30%. Subsequent application of corticotropin in the presence of nimodipine failed to produce an enhancement of I(Ca), suggesting that corticotropin acts selectively on L-type channels. In addition, corticotropin-mediated enhancement of I(Ca) after exposure to omega-conotoxin-GVIA and omega-agatoxin-IV was not significantly different from that observed in the control neurons, ruling out the involvement of N- and P/Q-type channels. The effect of corticotropin was mimicked by forskolin and (S(p))-cyclic adenosine 3',5'-monophosphothioate [(S(p))-cAMPS] and was significantly enhanced in the presence of phosphodiesterase or protein phosphatase inhibitors. On the other hand, the effect of corticotropin was markedly reduced in neurons intracellularly dialyzed with (R(p))-cAMPS, a regulatory site antagonist of cAMP-dependent protein kinase (PKA) or by extracellular perfusion of KT 5720, a catalytic site antagonist of PKA. Taken together, these results show for the first time that corticotropin enhances voltage-dependent Ca(2+) currents in brain neurons and that this increase is mediated through L-type channels and involves a cAMP-dependent mechanism.
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PMID:Selective enhancement of l-type calcium currents by corticotropin in acutely isolated rat amygdala neurons. 1117 56