Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Opioidergic modulation plays an important role in the control of oxytocin and vasopressin release by magnocellular neurons (MCNs) in the supraoptic and paraventricular nuclei of the hypothalamus. We have used whole cell patch-clamp recording in acute slices of the supraoptic nucleus (SON) of the hypothalamus to study opioidergic modulation of voltage-dependent K+ currents in MCNs that are involved in release activity. The mu-receptor agonist D-Ala2, N-Me-Phe4, Gly5-ol-enkephalin (DAMGO, 2 microM) affected K+ currents in 55% of magnocellular neurons recorded from. In these putative oxytocinergic cells, DAMGO increased the delayed rectifier current (IK(V)) amplitude by approximately 50% without significant effects on its activation kinetics. The transient A current (IA) was enhanced by DAMGO by approximately 36%. Its inactivation kinetic was accelerated slightly while the voltage dependence of steady-state inactivation was shifted by -6 mV to more negative potentials. All DAMGO effects were blocked by the preferential non-kappa-opioid antagonist naloxone (10 microM). The kappa-opioid agonist trans-(+/-)-3, 4-dichloro-N-methyl-N(2-[1-pyrrolidinyl]cyclohexyl)benzeneacetamide (U50,488; 10 microM) strongly suppressed IK(V) by approximately 57% and evoked a 20-mV hyperpolarizing shift and an acceleration of activation in both, DAMGO-sensitive and -insensitive putative vasopressinergic MCNs. U50,488 reduced IA by approximately 29% and tau of inactivation by -20% in DAMGO-sensitive cells. In contrast, in DAMGO-insensitive cells U50,488 increased IA by approximately 23% and strongly accelerated inactivation (tau -44%). The effects of U50,488 were suppressed by the selective kappa-receptor antagonist nor-binaltorphimine (5 microM). We conclude that mu- and kappa-opioidergic inputs decrease and increase excitability of oxytocinergic MCNs, respectively, through modulation of voltage-dependent K+ currents. In vasopressinergic MCNs, kappa-opioidergic inputs differentially modulate these K+ currents. The modulation of K+ currents is assumed to significantly contribute to opioidergic control of hormone release by MCNs within the supraoptic nucleus and from the axon terminals in the neural lobe.
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PMID:Opioidergic modulation of voltage-activated K+ currents in magnocellular neurons of the supraoptic nucleus in rat. 1020 Jan 98

The effects of opioid peptides on the osmotic release of neurohypophyseal hormones, arginine vasotocin (AVT) and mesotocin (MT), were determined in 2-day-old chicks. Experiment 1 examined the effect of a variety of doses of naloxone, an opioid antagonist, on chicks administered isotonic or hypertonic solution. Plasma osmolality in chicks administered hypertonic solution was significantly higher than that in groups administered isotonic solution. None of the doses of naloxone affected plasma osmolality in response to isotonic and hypertonic solution. Plasma levels of AVT increased in hypertonic solution and this response was further enhanced by naloxone injection as the doses increased. The hypertonic solution alone did not affect plasma levels of MT, but additional treatment with naloxone slightly increased plasma levels of MT. Experiment 2 examined the effect of DAMGO ([d-Ala(2), N-Me-Phe(4),Gly-ol]-enkepha lin), a specific mu receptor agonist. Relatively high plasma osmolality caused by hypertonic solution was not affected by additional treatment with DAMGO. Plasma levels of AVT in response to hypertonic solution and to additional treatment with naloxone were reduced by higher doses of DAMGO. Experiment 3 examined the effect of naloxone on chicks administered different concentrations of NaCl. Administration of hypertonic solution resulted in an increase in plasma osmolality and plasma levels of AVT. Naloxone administration enhanced the increase in plasma AVT levels in response to hypertonic solution. Experiment 4 examined the effect of naloxone on different kinds of hypertonic solution, 0.15 M NaCl, 1.5 M NaCl, 2.55 M urea, and 1.95 M sucrose. The increases in plasma osmolality resulting from the administration of the urea and sucrose solutions were the same as those in the chicks injected with 1.5 M NaCl. In sucrose-treated chicks, plasma levels of AVT increased in chicks administered naloxone but not in chicks injected with normal saline. In contrast, no significant changes in plasma levels of AVT were observed in urea treatment with or without naloxone. In Experiments 3 and 4, plasma levels of MT after administration of hypertonic solutions did not change. However, naloxone administration enhanced plasma levels of MT in osmotically stimulated chicks. The results of the present study suggest that opioid peptides attenuate the increase in plasma AVT and MT in hypertonic states.
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PMID:Effects of naloxone on neurohypophyseal peptide release by hypertonic stimulation in chicks. 1041 36

The activation of opioid receptors in neurones of the central nervous system leads to a variety of effects including the modulation of diuresis and parturition, processes that are directly controlled by the hypothalamic-neurohypophysial system (HNS). The effects of mu-opioid receptor activation on peptide release, voltage-gated Ca2+ currents and intracellular calcium levels ([Ca2+]i) were studied in isolated nerve terminals of the HNS. The mu-receptor agonist, DAMGO ([d-Ala2,N-Me-Phe4,Gly5-ol]-enkephalin) inhibited high K+-induced peptide release in a dose-dependent manner, with oxytocin release being more sensitive to block than vasopressin release at all concentrations tested. The addition of the mu-receptor antagonist CTOP (d-Phe-Cys-Tyr-d-Trp-Orn-Thr-Pen-Thr amide) was able to overcome the inhibitory effects of DAMGO. By contrast to previous results, voltage-gated Ca2+ currents were sensitive to blockage by DAMGO and this inhibition was also prevented by CTOP. Furthermore, [Ca2+]i measurements with Fura-2 corroborated the inhibition by DAMGO of calcium entry and its reversal by the micro -receptor antagonist in these nerve terminals. Thus, the decrease in neuropeptide release, particularly for oxytocin, induced by the activation of mu-opioid receptors in neurohypophysial terminals is mediated, at least in part, by a corresponding decrease in Ca2+ entry due to the inhibition of voltage-gated Ca2+ channels.
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PMID:mu-Opioid receptor modulates peptide release from rat neurohypophysial terminals by inhibiting Ca(2+) influx. 1289 84

Several approaches have been taken for these in vivo studies. In many studies, the use of semi-quantitative immuno-electron microscopy is the approach of choice. Endogenous opioid receptors display differential subcellular distributions with mu opioid receptor (MOPR) being mostly present on the plasma membrane and delta-opioid receptor (DOPR) and kappa-opioid receptor (KOPR) having a significant intracellular pool. Etorphine and DAMGO cause endocytosis of the MOPR, but morphine does not, except in some dendrites. Interestingly, chronic inflammatory pain and morphine treatment promote trafficking of intracellular DOPR to the cell surface which may account for the enhanced antinociceptive effects of DOPR agonists. KOPR has been reported to be associated with secretory vesicles in the posterior pituitary and translocated to the cell surface upon salt loading along with the release of vasopressin. The study of endogenous opioid receptors using in vivo models has produced some interesting results that could not have been anticipated in vitro. In vivo studies, therefore, are essential to provide insight into the mechanisms underlying opioid receptor regulation.
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PMID:In vivo trafficking of endogenous opioid receptors. 1893 Jul 41