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Oxytocin release from the rat neurohypophysis into the blood: effects of tachykinin NK-1 and NK-2 receptors agonists and antagonists

100%
Juszczak M., Boczek-Leszczyk E.
Journal of Physiology and Pharmacology
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2008
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tom 59
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nr 3
553-562
The aim of the present study was to investigate the effect of peptide NK-1 and NK-2 receptors agonists and antagonists (and their natural ligands, i.e., substance P and neurokinin A) on the oxytocin (OT) secretion from the rat neurohypophysis into the blood. Intracerebroventricular (icv) injection of substance P (SP) or highly selective NK-1 receptor agonist - [(Sar9,Met(O2)11)-Substance P] - significantly stimulated the OT secretion from the rat neurohypophysis into the general circulation. After icv injection of the NK-1 receptor antagonist - [(Tyr6,D-Phe7,D-His9)-Substance P (6-11)] - the blood plasma OT concentration was significantly lower, when compared to vehicle-injected animals. On the other hand, the icv administered neurokinin A (NKA) and the NK-2 receptor agonist - [(ß-Ala8)-Neurokinin A (4-10)] - were essentially inactive in modifying OT secretion. However, such injection of the NK-2 receptor antagonist - [(Tyr5,D-Trp6,8,9,Lys-NH210)-Neurokinin A (4-10)] - was found to diminish the blood plasma hormone concentration, when compared to vehicle-injected animals. The neurohypophysial content of OT was decreased in NKA-treated rats, but neither the NK-2 receptor agonist nor antagonist were able to affect the OT output from the rat posterior pituitary. The hypothalamic levels of OT were not modified by any of the studied peptides. The present data strongly indicate a major role for the tachykinin NK-1 receptor in SP- and/or NKA-dependent regulation of OT secretion from the rat neurohypophysis into the blood.
2
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Role of tachykinin receptors and melatonin in oxytocin secretion from isolated rat hypothalamo-neurohypophysial system

100%
Juszczak M., Furykiewicz-Nykis K., Stempniak B.
Journal of Physiology and Pharmacology
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2004
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tom 55
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nr 4
Present investigations were undertaken to study the influence of peptide NK-1 and NK-2 receptor agonists and antagonists as well as substance P and neurokinin A (the natural ligands for these tachykinin receptors) on oxytocin (OT) release from isolated rat hypothalamo-neurohypophysial (H-N) system as well as to determine whether the tachykinin NK-1 and/or NK-2 receptors contribute to the response of oxytocinergic neurons to melatonin. The results show, for the first time, that highly selective NK-1 receptor agonist, i.e., [Sar9,Met(O2)11]-Substance P, enhances while the NK-1 receptor antagonist (Tyr6,D-Phe7,D-His9)-Substance P (6-11) - sendide - diminishes significantly OT secretion; the latter peptide was also found to antagonize the substance P-induced hormone release from isolated rat H-N system, when used at the concentration of 10-7 M/L. Melatonin significantly inhibited basal and substance P-stimulated OT secretion. Neurokinin A and the NK-2 receptor selective agonist (ß-Ala8)-Neurokinin A (4-10) as well as the NK-2 receptor antagonist (Tyr5,D-Trp6,8,9, Lys-NH210)-Neurokinin A (4-10) were essentially inactive in modifying OT release from the rat H-N system in vitro. The present data indicate a distinct role for tachykinin NK-1 (rather than NK-2) receptor in tachykinin-mediated regulation of OT secretion from the rat H-N system. Under present experimental conditions, however, a role of respective tachykinin receptors in the response of oxytocinergic neurons to melatonin has not been found.
3
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Effect of melatonin on the vasopressin secretion as influenced by tachykinin NK-1 receptor agonist and antagonist: in vivo and in vitro studies

80%
Juszczak M., Boczek-Leszczyk E., Stempniak B.
Journal of Physiology and Pharmacology
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2007
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tom 58
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nr 4
The aim of the present study was to investigate the influence of melatonin on vasopressin (AVP) release from the rat hypothalamo-neurohypophysial (H-NH) system, both in vivo and in vitro, possibly modified by the peptide NK-1 and/or NK-2 receptor agonists and antagonists. Highly selective NK-1 receptor agonist, i.e., [Sar9,Met(O2)11]-Substance P, has been shown to enhance the AVP release from isolated rat H-NH system in vitro, while the NK-1 receptor antagonist - (Tyr6,D-Phe7,D-His9)-Substance P (6-11) as well as the NK-2 receptor selective agonist - (ß-Ala8)-Neurokinin A (4-10) and antagonist - (Tyr5,D-Trp6,8,9,Lys-NH210)-Neurokinin A (4-10) were essentially inactive in modifying AVP secretion. Melatonin inhibited basal release of AVP but was not able to reduce significantly the in vitro response of vasopressinergic neurones to NK-1 receptor agonist. After intracerebroventricular (icv) administration, substance P (SP), neurokinin A (NKA) and the NK-1 receptor agonist (all at the concentration of 10-7 M/L) significantly enhanced plasma AVP concentration. Such stimulatory effect of the latter peptide on AVP output from the neurohypophysis was reduced by an intravenous (iv) injection of melatonin, which itself (at a concentration of 5 ng/ml) caused a significant decrease in AVP release 10 min after injection. The inhibitory influence of melatonin on the AVP secretion was absent in rats injected icv with both tachykinin receptors antagonists, the NK-2 receptor agonist or NKA. The present data indicate a distinct role for NK-1 receptor in NKA/SP-mediated regulation of AVP release from the rat H-NH system. They have also shown that, under present experimental conditions, the stimulatory effect of NK-1 receptor activation on AVP secretion into the blood is sensitive to inhibitory influence of melatonin.
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