Nitric oxide synthase content of hypothalamic explants: increase by norepinephrine and inactivated by NO and cGMP.

Canteros, Griselda; Rettori, Valéria; Genaro, Ana Marı́a; Suburo, Ángela M.; Gimeno, M.F.; McCann, S. M.

doi:10.1073/pnas.93.9.4246

Cited by 68 publications

(45 citation statements)

References 15 publications

(10 reference statements)

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“…We further confirmed that we actually had increased the content of enzyme by isolating the enzyme according to the method of Bredt and Snyder (20) and then measuring the conversion of labeled arginine to citrul-line. The conversion was significantly increased by NE (19).…”

Section: Role Of No In Control Of Lhrh Releasementioning

confidence: 82%

“…Furthermore, high concentrations of cGMP released by NO also acted in the explants or even in the homogenates to suppress the activation of NOS. This pathway could also be active in the presence of high concentrations of NO, such as would occur in infection by induction of inducible NOS by bacterial or viral products (19).…”

Section: Role Of No In Control Of Lhrh Releasementioning

confidence: 99%

“…PLA 2 causes the conversion of membrane phospholipids in the LHRH terminal to arachidonate, which then can be converted to PGE 2 via the activated cyclooxygenase. The released PGE 2 activates adenyl cyclase causing an increase in cAMP release, which activates protein kinase-A, leading to exocytosis of LHRH secretory granules into the hypophyseal portal capillaries for transmission to the anterior pituitary gland (19).…”

Section: Role Of No In Control Of Lhrh Releasementioning

confidence: 99%

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The role of nitric oxide in reproduction

McCann

Mastronardi

Walczewska

et al. 1999

Braz J Med Biol Res

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Nitric oxide (NO) plays a crucial role in reproduction at every level in the organism. In the brain, it activates the release of luteinizing hormone-releasing hormone (LHRH). The axons of the LHRH neurons project to the mating centers in the brain stem and by afferent pathways evoke the lordosis reflex in female rats. In males, there is activation of NOergic terminals that release NO in the corpora cavernosa penis to induce erection by generation of cyclic guanosine monophosphate (cGMP). NO also activates the release of LHRH which reaches the pituitary and activates the release of gonadotropins by activating neural NO synthase (nNOS) in the pituitary gland. In the gonad, NO plays an important role in inducing ovulation and in causing luteolysis, whereas in the reproductive tract, it relaxes uterine muscle via cGMP and constricts it via prostaglandins (PG).

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Section: Role Of No In Control Of Lhrh Releasementioning

confidence: 82%

Section: Role Of No In Control Of Lhrh Releasementioning

confidence: 99%

Section: Role Of No In Control Of Lhrh Releasementioning

confidence: 99%

See 1 more Smart Citation

The role of nitric oxide in reproduction

McCann

Mastronardi

Walczewska

et al. 1999

Braz J Med Biol Res

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“…The content of NOS in the tissue at the end of the experiments was estimated by the modified citrulline method (10). Because arginine is converted by NOS in the presence of O 2 and cofactors into equimolar concentrations of citrulline that remains in the tissue and NO that rapidly degrades, measurement of [ 14 C]citrulline produced from [ 14 C]arginine added to the homogenized muscle provides a convenient measure of the activity of NOS.…”

Section: Metabolism Of [ 14 C]arachidonic Acidmentioning

confidence: 99%

Nitric oxide in the contractile action of bradykinin, oxytocin, and prostaglandin F ₂ α in the estrogenized rat uterus

Chaud¹,

Franchi²,

Rettori³

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

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Experiments were performed on uteri from estrogen-primed female rats. Bradykinin (BK) (10 ؊8 M) significantly augmented biosynthesis of prostaglandin F 2 ␣ (PGF 2 ␣) and prostaglandin E 2 (PGE 2 ), and this synthesis was completely blocked by N G -monomethyl L-arginine (NMMA) (300 M), a competitive inhibitor of nitric oxide synthase (NOS). Blockade of prostaglandin synthesis by indomethacin caused rapid dissipation of isometric developed tension (IDT) induced by BK. Blockade of NOS with NMMA had similar but less marked effects. Combining the two inhibitors produced an even more rapid decay in IDT, suggesting that BK-induced NO release maintains IDT by release of prostanoids. The decline of frequency of contraction (FC) was not significantly altered by either indomethacin or NMMA but was markedly accelerated by combination of the inhibitors, which suggests that PGs maintain FC and therefore FC decline is accelerated only when PG production is blocked completely by combination of the two inhibitors of PG synthesis. The increase in IDT induced by oxytocin was unaltered by indomethacin, NMMA or their combination indicating that neither NO nor PGs are involved in the contractions induced by oxytocin. However, the decline in FC with time was significantly reduced by the inhibitor of NOS, NMMA, suggesting that FC decay following oxytocin is caused by NO released by the contractile process. In the case of PGF 2 ␣, NMMA resulted in increased initial IDT and FC. The decline in FC was rapid and dramatically inhibited by NMMA. Receptor-mediated contraction by BK, oxytocin, and PGF 2 ␣ is modulated by NO that maintains IDT by releasing PGs but reduces IDT and FC via cyclic GMP.Nitric oxide (NO), a soluble gas, is synthesized by endothelial NO synthase (NOS), a constitutive enzyme that converts arginine to the free radical NO plus citrulline in the presence of NADPH and other cofactors. Endothelial (NOS) is a constitutive enzyme in vascular endothelial cells, it is activated by cholinergic stimulation. The NO produced diffuses to overlying vascular smooth muscle and activates soluble guanylate cyclase with the subsequent formation of cyclic GMP (cGMP) (1). NO interacts with the heme group in soluble guanylate cyclase altering its conformation, thereby activating the enzyme that converts guanine triphosphate into cGMP. cGMP then relaxes the overlying smooth muscle (2).Another constitutive isoform of NOS, neural (n) NOS, has been found in various parts of the central and peripheral nervous systems where it acts as a gaseous neurotransmitter (3, 4). In the hypothalamus, it activates the release of luteinizing hormone-releasing hormone that induces sexual behavior on the one hand, and release of luteinizing hormone on the other, both of which are required for reproduction (5, 6).In the periphery, terminals of NOergic neurons are also present in the corpora cavernosa penis and release of NO from these terminals activates guanylate cyclase in the smooth muscle causing relaxation, a requirement for penile erection (7). In ut...

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“…In studies not related to fever research, it has been shown that norepinephrine (NE) activates e-, n-, and iNOS in brain (1,8,21). Thus, in the case of the control of the release of luteinizing hormone-releasing hormone (LHRH) from the hypothalamus, the NE-induced increased activity of NOS has been specifically attributed to the activation of ␣ 1 -adrenoceptors (AR) on NOergic neurons (8).…”

mentioning

confidence: 99%

Preoptic nitric oxide attenuates endotoxic fever in guinea pigs by inhibiting the POA release of norepinephrine

Feleder¹,

Perlik²,

Blatteis³

2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Lipopolysaccharide (LPS) administration induces hypothalamic nitric oxide (NO); NO is antipyretic in the preoptic area (POA), but its mechanism of action is uncertain. LPS also stimulates the release of preoptic norepinephrine (NE), which mediates fever onset. Because NE upregulates NO synthases and NO induces cyclooxygenase (COX)-2-dependent PGE2, we investigated whether NO mediates the production of this central fever mediator. Conscious guinea pigs with intra-POA microdialysis probes received LPS intravenously (2 μg/kg) and, thereafter, an NO donor (SIN-1) or scavenger (carboxy-PTIO) intra-POA (20 μg/μl each, 2 μl/min, 6 h). Core temperature (Tc) was monitored constantly; dialysate NE and PGE2 were analyzed in 30-min collections. To verify the reported involvement of α2-adrenoceptors (AR) in PGE2 production, clonidine (α2-AR agonist, 2 μg/μl) was microdialyzed with and without SIN-1 or carboxy-PTIO. To assess the possible involvement of oxidative NE and/or NO products in the demonstrated initially COX-2-independent POA PGE2 increase, (+)-catechin (an antioxidant, 3 μg/μl) was microdialyzed, and POA PGE2, and Tc were determined. SIN-1 and carboxy-PTIO reduced and enhanced, respectively, the rises in NE, PGE2, and Tc produced by intravenous LPS. Similarly, they prevented and increased, respectively, the delayed elevations of PGE2 and Tc induced by intra-POA clonidine. (+)-Catechin prevented the LPS-induced elevation of PGE2, but not of Tc. We conclude that the antipyretic activity of NO derives from its inhibitory modulation of the LPS-induced release of POA NE. These data also implicate free radicals in POA PGE2 production and raise questions about its role as a central LPS fever mediator.

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Nitric oxide synthase content of hypothalamic explants: increase by norepinephrine and inactivated by NO and cGMP.

Abstract: Release of luteinizing hormone (LH)-releasing hormone (LHRH), the hypothalamic peptide that controls release of LH from the adenohypophysis, is controlled by NO Since citrulline remains in the sample, whereas the equimolar

Cited by 68 publications

References 15 publications

The role of nitric oxide in reproduction

The role of nitric oxide in reproduction

Nitric oxide in the contractile action of bradykinin, oxytocin, and prostaglandin F ₂ α in the estrogenized rat uterus

Preoptic nitric oxide attenuates endotoxic fever in guinea pigs by inhibiting the POA release of norepinephrine

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Nitric oxide synthase content of hypothalamic explants: increase by norepinephrine and inactivated by NO and cGMP.

Abstract: Release of luteinizing hormone (LH)-releasing hormone (LHRH), the hypothalamic peptide that controls release of LH from the adenohypophysis, is controlled by NO Since citrulline remains in the sample, whereas the equimolar

Cited by 68 publications

References 15 publications

The role of nitric oxide in reproduction

The role of nitric oxide in reproduction

Nitric oxide in the contractile action of bradykinin, oxytocin, and prostaglandin F 2 α in the estrogenized rat uterus

Preoptic nitric oxide attenuates endotoxic fever in guinea pigs by inhibiting the POA release of norepinephrine

Contact Info

Product

Resources

About

Nitric oxide in the contractile action of bradykinin, oxytocin, and prostaglandin F ₂ α in the estrogenized rat uterus