The Role of Prostaglandins in Neuroendocrine Junctions:Studies in the Pineal Gland and the Hypothalamus

Cardinali, Daniel P.; Ritta, Mónica N.

doi:10.1159/000123452

Cited by 29 publications

(10 citation statements)

References 66 publications

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“…Other investigators have also shown that activation of pineal ai-adrenergic receptors affects pi neal function. For example, agonists of these receptors in crease pineal prostaglandins [3] and also increase the effect of |3-adrenoreceptor agonists on induction of the enzyme serotonin-N-acetyltransferase [17][18][19]. The results of the present study are consistent with these findings, especially the latter, since 5-HT antagonizes the stimulatory effect of NE on cyclic adenosine monophosphate in pineal [28].…”

Section: Discussionsupporting

confidence: 87%

Alpha-Adrenergic Control of Serotonin Release from Rat Pineal Glands

Aloyo

Walker

1988

Neuroendocrinology

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This study was designed to determine if norepinephrine (NE) stimulated release of pineal serotonin (5-HT) is receptor mediated and to identify the receptor(s) most influential in the release process. Efflux of ³H-5-HT from rat pineals in vitro was significantly increased within 5 min after NE was added to perifusion buffer in concentrations ranging from 0.1 to 3 µM³H-5-HT was not simply displaced from pinealocytes by NE, since buffer containing 3 µM 5-HT had no effect on ³H-5-HT efflux. Furthermore, NE enhanced ³H-5-HT secretion by a stereospecific process, since d-NE was significantly less effective than l-NE. The α₁-adrenoreceptor agonists phenylephrine and cirazoline simulated the effects of NE, significantly increasing ³H-5-HT efflux in single and sequential stimulations. Furthermore, the α₁-adrenergic receptor antagonist prazosin reduced NE-stimulated release of ³H-5-HT. In contrast, the α₂- and β-adrenoreceptor agonists naphazoline or clonidine and isoproterenol, respectively, were without effect. In addition, the α₂- and the β-receptor antagonists rauwolscine and timolol, respectively, had no effect on NE-stimulated release of pineal 5-HT. In conclusion, the data show that NE stimulates 5-HT release within minutes from rat pineal glands in vitro. Unlike the pineal mechanism controlling melatonin synthesis, which has a longer latency and requires β-adrenergic receptor activation, 5-HT release is regulated by activation of αi-receptors. Thus, the pineal may be useful model for studying how separate intracellular processes are controlled by common neural stimuli.

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Section: Discussionsupporting

confidence: 87%

Alpha-Adrenergic Control of Serotonin Release from Rat Pineal Glands

Aloyo

Walker

1988

Neuroendocrinology

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“…Activation of PGE2 synthesis is considered an essential step in the sequence of events leading to LHRH release from hypothalamic nerve terminals [6,22,27], This activa tion appears to be effected mainly by norepinephrine (NE) [5,8,25] even though epinephrine and dopamine are also capable of inducing some PGE2 release [25]. NE interacts with a-adrenergic receptors to stimulate the release of PGE2, which in turn induces LHRH release [28].…”

Section: Discussionmentioning

confidence: 99%

Release of Prostaglandin E<sub>2</sub> from the Hypothalamus Depends on Extracellular Ca<sup>2+</sup> Availability: Relation to LHRH Release

Ojeda¹,

Negro‐Vilar²

1984

Neuroendocrinology

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The present experiments were performed to investigate the role of extracellular Ca²⁺ in the process of prostaglandin E₂ (PGE₂) release from the median eminence (ME) of the hypothalamus. Changes in the release of LHRH were also evaluated. Incubation of ME fragments with different concentrations of K⁺ induced a dose-related increase in PGE₂ and LHRH release. The effect of K⁺ depended upon the Ca²⁺ concentration in the incubation medium. A Ca²⁺ concentration of 0.1 mM was sufficient to permit a significant response in both PGE₂ and LHRH release to K⁺. The effect of a maximal K⁺ concentration (56 mM)was almost completely obliterated by omitting Ca²⁺ from the incubation medium and by chelating the remaining Ca²⁺ with EDTA or EGTA. The Ca²⁺ ionophore A23187, tested at different concentrations (1–50 µM) significantly increased the release of both PGE₂ and LHRH from the ME in a Ca²⁺-dependent manner. A Ca²⁺ concentration of 0.25 mM allowed maximal LHRH response to the ionophore, but permitted only a partial (50%) PGE₂ response. Blockade of Ca²⁺ channels with Verapamil, a Ca²⁺ entry blocker, prevented the effect of K⁺ on both PGE₂ and LHRH release in a dose-dependent manner. The results demonstrate that release of PGE₂ from ME nerve terminals depends upon the concentration of extracellular Ca²⁺ and suggest that PGE₂ release is initiated by an increase in Ca²⁺ influx to the terminals. In addition, the data provide further evidence that release of LHRH is, to a significant extent, a function of Ca²⁺ influx through Ca²⁺ voltage-dependent channels.

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“…) and these are involved in the reduction by melatonin of free radical formation by mitochondria (Acuna‐Castroviejo et al . ), cyclooxygenase (COX) during prostaglandin synthesis (Cardinali & Ritta, ), and uncoupled nitric oxide synthase (NOS) (Tapias et al . ).…”

Section: Introductionmentioning

confidence: 99%

“…Melatonin scavenges hydroxyl (Poeggeler et al 1993), carbonate (Hardeland et al 2003) and peroxynitrite (Hardeland et al 2007) radicals by receptor-independent mechanisms, probably involving its aromatic indole ring structure. Classical G-protein-coupled melatonin receptors occur in the cardiovascular system (Dubocovich & Markowska, 2005;Paulis et al 2012) and these are involved in the reduction by melatonin of free radical formation by mitochondria (Acuna-Castroviejo et al 2007), cyclooxygenase (COX) during prostaglandin synthesis (Cardinali & Ritta, 1983), and uncoupled nitric oxide synthase (NOS) (Tapias et al 2009). Melatonin also acts via its receptors to stimulate production of free radical scavengers such as superoxide dismutase, catalase and glutathione peroxidase and reductase (López et al 2006).…”

Section: Introductionmentioning

confidence: 99%

Maternal melatonin administration mitigates coronary stiffness and endothelial dysfunction, and improves heart resilience to insult in growth restricted lambs

Tare

Parkington

Wallace

et al. 2014

The Journal of Physiology

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Key pointsr Failure of the placenta to develop and perform gives rise to intrauterine growth restriction (IUGR) in the fetus. IUGR is associated with impaired heart function in childhood and can even persist long term.r Oxidative stress is increased in IUGR and we asked if an antioxidant could reduce this.Melatonin is a well-known and well-studied hormone, present in all of us, and it has potent antioxidant properties.r In this study we administered melatonin to pregnant ewes carrying twins, one with IUGR. r Maternal melatonin improved oxygen delivery to the IUGR fetus and strengthened and protected its heart against infarct. After birth, the poor function and stiffness in the coronary arteries of IUGR lambs were entirely prevented by melatonin.r Our results demonstrate that administration of melatonin to a mother carrying an IUGR fetus can markedly dampen the adverse heart and artery effects in the offspring following birth.Abstract Intrauterine growth restriction (IUGR) is associated with impaired cardiac function in childhood and is linked to short-and long-term morbidities. Placental dysfunction underlies most IUGR, and causes fetal oxidative stress which may impact on cardiac development. Accordingly, we investigated whether antenatal melatonin treatment, which possesses antioxidant properties, may afford cardiovascular protection in these vulnerable fetuses. IUGR was induced in sheep fetuses using single umbilical artery ligation on day 105-110 of pregnancy (term 147). Study 1: melatonin (2 mg h −1 ) was administered I.V. to ewes on days 5 and 6 after surgery. On day 7 fetal heart function was assessed using a Langendorff apparatus. Study 2: a lower dose of melatonin (0.25 mg h −1 ) was administered continuously following IUGR induction and the ewes gave birth normally at term. Lambs were killed when 24 h old and coronary vessels studied. Melatonin significantly improved fetal oxygenation in vivo. Contractile function in the right ventricle and coronary flow were enhanced by melatonin. Ischaemia-reperfusion-induced infarct area was 3-fold greater in IUGR hearts than in controls and this increase was prevented by melatonin. In isolated neonatal coronary arteries, endothelium-dependent nitric oxide (NO) bioavailability was reduced in IUGR, and was rescued by modest melatonin treatment. Melatonin exposure also induced the emergence of an indomethacin-sensitive vasodilation. IUGR caused marked stiffening of the coronary artery and this was prevented by melatonin. Maternal melatonin treatment reduces fetal hypoxaemia, improves heart function and coronary blood flow and rescues cardio-coronary deficit induced by IUGR.(Received 9 January 2014; accepted after revision 3 April 2014; first published online 7 April 2014) Corresponding author H. C. Parkington: Department of Physiology, Monash University, Wellington Road, Clayton, VIC 3800, Australia. Email: helena.parkington@monash.eduAbbreviations BK, bradykinin; COX, cyclooxygenase; EDHF, endothelium-derived hyperpolarizing factor; eNOS, endothelial nitric oxide syn...

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The Role of Prostaglandins in Neuroendocrine Junctions:Studies in the Pineal Gland and the Hypothalamus

Cited by 29 publications

References 66 publications

Alpha-Adrenergic Control of Serotonin Release from Rat Pineal Glands

Alpha-Adrenergic Control of Serotonin Release from Rat Pineal Glands

Release of Prostaglandin E<sub>2</sub> from the Hypothalamus Depends on Extracellular Ca<sup>2+</sup> Availability: Relation to LHRH Release

Maternal melatonin administration mitigates coronary stiffness and endothelial dysfunction, and improves heart resilience to insult in growth restricted lambs

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