Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20366 (substance P)
 21,176 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of melatonin on tension of isolated bovine pulmonary vascular and bronchial smooth muscle rings were examined in these experiments. Melatonin caused a dose-dependent relaxation of precontracted (30 mM KCl) pulmonary artery and vein, although the effect is greater in arterial smooth muscle. This relaxant response was blocked by preincubating vessels with antagonists of vasoactive intestinal peptide or Substance P. In bronchial smooth muscle, melatonin caused a small contractile response. These experiments demonstrate that in response to melatonin the pulmonary vasculature relaxes, while in airway smooth muscle the reverse, constriction, occurs. It is hypothesized that nocturnal exaggeration of asthma may, in part, be due to changes in circulating levels of melatonin.
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PMID:Influence of melatonin on bovine pulmonary vascular and bronchial airway smooth muscle tone. 754 81

The influence of several classes of drugs on the melatonin-induced vasorelaxation of isolated rat aorta were examined. Melatonin caused a dose-dependent relaxation of precontracted (30 mM KCl) aorta. This relaxant response was blocked by preincubating vessels with antagonists of vasoactive intestinal peptide. Substance P antagonists did not alter the response to melatonin. Pretreatment of vessels with 6-hydroxydopamine, lidocaine, or tetrodotoxin antagonized the relaxant response to melatonin. On the other hand, pretreatment with atropine + propranolol did not alter the response to melatonin. These experiments suggest that melatonin may exert part of its vasoactive actions by an interaction with perivascular nerve terminals.
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PMID:Pharmacologic studies on the mechanism of melatonin-induced vasorelaxation in rat aorta. 875 Mar 47

The suprachiasmatic nucleus (SCN) harbors an endogenous oscillator generating circadian rhythms that are synchronized to the external light/dark cycle by photic information transmitted via the retinohypothalamic tract (RHT). The RHT has recently been shown to contain pituitary adenylate cyclase-activating polypeptide (PACAP) as neurotransmitter/neuromodulator. PACAPergic effects on cAMP-mediated signaling events in the SCN are restricted to distinct time windows and sensitive to melatonin. In neurons isolated from the SCN of neonatal rats we investigated by means of the fura-2 technique whether PACAP and melatonin also influence the intracellular calcium concentration ([Ca2+]i). PACAP elicited increases of [Ca2+]i in 27% of the analyzed neurons, many of which were also responsive to the RHT neurotransmitters glutamate and/or substance P. PACAP-induced changes of [Ca2+]i were independent of cAMP, because they were not mimicked by forskolin or 8-bromo-cAMP. PACAP caused G-protein- and phospholipase C-mediated calcium release from inositol-trisphosphate-sensitive stores and subsequent protein kinase C-mediated calcium influx, demonstrated by treatment with GDP-beta-S, neomycin, U-73122, calcium-free saline, thapsigargin, bisindolylmaleimide, and chelerythrine. The calcium influx was insensitive to antagonists of voltage-gated calcium channels of the L-, N-, P-, Q- and T-type (diltiazem, nifedipine, verapamil, omega-conotoxin, omega-agatoxin, amiloride). Immunocytochemical characterization of the analyzed cells revealed that >50% of the PACAP-sensitive neurons were GABA-immunopositive. Our data demonstrate that in the SCN PACAP affects the [Ca2+]i, suggesting that different signaling pathways (calcium as well as cAMP) are involved in PACAPergic neurotransmission or neuromodulation. Melatonin did not interfere with calcium signaling, indicating that in SCN neurons the hormone primarily affects the cAMP signaling pathway.
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PMID:Pituitary adenylate cyclase-activating polypeptide and melatonin in the suprachiasmatic nucleus: effects on the calcium signal transduction cascade. 987 Sep 51

Previous data showed that aging of the central nervous system (CNS) is associated with widespread changes in tachykinin gene expression. However, there are no data about the possible role of exogenous melatonin in modulating the tachykinergic system during aging. The aim of this work was to analyze the age-dependent changes on neurokinin A (NKA) and substance P (SP) levels in hypothalamus, pituitary, pineal gland and striatum and the role of exogenous melatonin on these changes. We studied female rats at three different ages: 5-month-old (cyclic), 15-month-old (preacyclic) and 25-month-old (acyclic). Hypothalamic tachykinin levels increase when female rats reached acyclicity, this increase was blunted in acyclic-melatonin-treated rats. However, melatonin treatment in young cyclic rats resulted in significantly increased values as compared to controls. Pituitary NKA concentrations did no show age-dependent changes in control rats, however, in both, preacyclic and acyclic-melatonin-treated rats significantly increased values of pituitary NKA were found compared to controls. In the pineal gland, a marked decrease of NKA levels was observed in acyclic-control rats. Melatonin treatment did not alter this decrease. In the striatum, NKA and SP concentrations were significantly reduced in preacyclic- and acyclic-control rats compared to young cyclic rats, melatonin had no effect on striatal tachykinins. Our results indicate that melatonin may regulate tachykinin stores during aging mainly on structures of the neuroendocrine-reproductive axis.
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PMID:Age differences in neurokinin A and substance P from the hypothalamus, pituitary, pineal gland, and striatum of the rat. Effect of exogenous melatonin. 1208 26

Mammalian neurokinin A (NKA) and substance P (SP) are neuropeptides widely distributed in the body; they are potential regulators of the basal blood flow and therefore of the function of many organs and tissues. In the present investigation, we studied the age-dependent changes in NKA and SP in ovary, liver, pancreas and spleen as well as the role of exogenous melatonin on these changes. Female rats of 5, 15 or 25 months of age were studied. In the ovary, NKA concentrations did not change during aging. SP concentrations in the control group were significantly higher (P<0.01) in old rats than in the other two age groups studied. Melatonin treatment resulted in reduced concentrations as compared with those of the control old rats. In the pancreas, NKA and SP concentrations increased during aging, the young rats showing significantly lower values (P<0.01) than middle-aged and old rats for NKA and significantly lower (P<0.01) than the old rats for SP. After melatonin treatment the differences in NKA concentrations disappeared and SP decreased in middle-aged as compared with those in old rats. In the liver, NKA and SP concentrations in the control and melatonin-treated groups did not differ significantly for the three age groups studied. Splenic NKA in control and melatonin-treated groups increased from young to middle-age up to old ages. SP concentrations showed similar values at all ages except in melatonin-treated old rats; in these animals there were significantly higher concentrations than in young melatonin-treated rats. The effect of melatonin was mainly observed on the ovary and pancreas in old rats, with a reduction in the concentrations as compared with those observed in the young groups.
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PMID:Developmental pattern of tachykinins during aging in several organs: effect of exogenous melatonin. 1221 22

The aim of the present investigations was to study the influence of substance P (a member of a family of peptides known as tachykinins) on basal and K(+)-evoked vasopressin (AVP) and oxytocin (OT) release from rat hypothalamo-neurohypophysial system in vitro as well as to determine whether this effect of substance P is sensitive to melatonin. The present results show that substance P stimulates basal AVP and OT release from isolated hypothalamo-neurohypophysial system, when used at the concentrations of 10(-6) and 10(-7)M/l. At the concentration of 10(-9)M/l, however, substance P was found to stimulate the in vitro secretion of AVP, but not that of OT. Melatonin diminished basal release of AVP; it also significantly inhibited the substance P-stimulated secretion of AVP and OT. K(+)-evoked release of the neurohypophysial hormones was not further modified by either substance P or melatonin. The present results show that the stimulatory effect of substance P on basal release of AVP and OT from rat hypothalamo-neurohypophysial system in vitro is sensitive to inhibitory influence of melatonin.
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PMID:Melatonin inhibits the substance P-induced secretion of vasopressin and oxytocin from the rat hypothalamo-neurohypophysial system: in vitro studies. 1250 91

The aim of this study was to investigate a possible role of neurokinin A (a member of a family of peptides known as tachykinins) in the pineal-neurohypophysial interrelationship. The effect of neurokinin A (NKA) alone or in the presence of pineal hormone - melatonin on basal and K(+)-stimulated vasopressin and oxytocin secretion from the hypothalamo-neurohypophysial system was studied in vitro. The present results show that NKA stimulated basal vasopressin and oxytocin release from the isolated hypothalamo-neurohypophysial system, when used at the concentration of 10(-7) M/L. Melatonin diminished basal release of the neurohypophysial hormones; it also significantly inhibited the NKA-stimulated secretion of vasopressin and oxytocin. Lower concentrations of NKA did not affect the neurohypophysial hormones basal release, however, when melatonin was added to the medium enriched with NKA at the concentration of 10(-9) M/L, the vasopressin secretion from the hypothalamo-neurohypophysial explants was decreased significantly. The K(+)-evoked release of neurohypophysial hormones was not further modified by either NKA or melatonin. The present results confirm previous reports as to the inhibitory effect of melatonin on both vasopressin and oxytocin secretion from the hypothalamo-neurohypophysial complex in vitro. However, under present experimental conditions, the contribution of NKA in the mechanisms of pineal-neurohypophysial interrelationships has not been demonstrated.
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PMID:Neurokinin A and the neurohypophysial response to melatonin: in vitro studies. 1251 Aug 66

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., [Sar(9),Met(O(2))(11)]-Substance P, enhances while the NK-1 receptor antagonist (Tyr(6),D-Phe(7),D-His(9))-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 (beta-Ala(8))-Neurokinin A (4-10) as well as the NK-2 receptor antagonist (Tyr(5),D-Trp(6,8,9),Lys-NH(2)(10))-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.
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PMID:Role of tachykinin receptors and melatonin in oxitocin secretion from isolated rat hypothalmo-neurohypophysial system. 1561 40

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., [Sar(9),Met(O(2))(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--(Tyr(6),DPhe(7),D-His(9))-Substance P (6-11) as well as the NK-2 receptor selective agonist--(beta-Ala(8))-Neurokinin A (4-10) and antagonist--(Tyr(5),D-Trp(6,8,9),Lys-NH(2)(10))-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 eurohypophysis 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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PMID:Effect of melatonin on the vasopressin secretion as influenced by tachykinin NK-1 receptor agonist and antagonist: in vivo and in vitro studies. 1819 91

Seasonally breeding mammals such as sheep use photoperiod, encoded by the nocturnal secretion of the pineal hormone melatonin, as a critical cue to drive hormone rhythms and synchronize reproduction to the most optimal time of year. Melatonin acts directly on the pars tuberalis (PT) of the pituitary, regulating expression of thyrotropin, which then relays messages back to the hypothalamus to control reproductive circuits. In addition, a second local intrapituitary circuit controls seasonal prolactin (PRL) release via one or more currently uncharacterized low-molecular-weight peptides, termed "tuberalins," of PT origin. Studies in birds have identified the transcription factor Eya3 as the first molecular response activated by long photoperiod (LP). Using arrays and in situ hybridization studies, we demonstrate here that Eya3 is the strongest LP-activated gene in sheep, revealing a common photoperiodic molecular response in birds and mammals. We also demonstrate TAC1 (encoding the tachykinins substance P and neurokinin A) to be strongly activated by LP within the sheep PT. We show that these PRL secretagogues act on primary pituitary cells and thus are candidates for the elusive PT-expressed tuberalin seasonal hormone regulator.
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PMID:Identification of Eya3 and TAC1 as long-day signals in the sheep pituitary. 2043 41


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