Nitric oxide modulates the release of vasopressin from rat hypothalamic explants.

Yasin, Sharifah A.; Costa, Alfredo; Trainer, Peter; Windle, Richard; Forsling, Mary L.; Grossman, Ashley

doi:10.1210/endo.133.3.7689960

Cited by 108 publications

(43 citation statements)

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“…The administration of NO donors and NOS antagonists in vivo induce changes in pituitary-gonadal [3], pituitary-adrenal [4, 5] and the neurohypophyseal axes [6], while NO antagonism enhances the responsiveness of the hypothalamo-pituitary-adrenal (HPA) axis to endotoxin administration [4, 5]. This is compatible with other data demonstrating inhibitory modulation by NO of the central regulators of the HPA, corticotropin-releasing hormone (CRH) [7] and vasopressin [8]. Similarly, we have shown that the generation of CO in hypothalamic explants inhibits the secretion of CRH [9] and vasopressin [10].…”

Section: Introductionsupporting

confidence: 75%

Endotoxin Induces Interleukin-1β and Nitric Oxide Synthase mRNA in Rat Hypothalamus and Pituitary

et al. 1998

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The gases nitric oxide (NO) and carbon monoxide (CO) may be involved in hypothalamo-pituitary-adrenal axis (HPA) modulation. In the brain, NO is synthesized by two forms of NO synthase (NOS), a constitutive neuronal form (nNOS) and an inducible form (iNOS). There are also a constitutive heme oxygenase (HO₂) and an inducible form (HO₁) which generate CO. We have therefore investigated the effect of peripheral lipopolysaccharide (LPS) administration on the gene expression of these enzymes along with interleukin-1β (IL-1β) gene expression in the hypothalamus, pituitary and liver. Male Wistar rats (200–250 g body weight) were injected intraperitoneally with endotoxin (Escherichia coli, 055 B5) dissolved in sterile normal saline [250 µg/kg first group, 2.5 mg/kg (second group) and 6.25 mg/kg (third group)] in a final volume of 0.5 ml, or saline alone in the control group. The first and the second groups were studied 1, 3, 8 and 24 h after LPS (n = 4 per group); the third group was studied at 3 h. Total RNA was extracted from the hypothalamus, pituitary and liver, and cDNA was made using standard reverse transcriptase methods. Duplex polymerase chain reaction (PCR) was standardised in order to quantify the expression of a specific gene in relation to the ‘house-keeping’ gene β-actin. The specific genes studied were iNOS, nNOS, HO₁, HO₂ and IL-1β. The PCR products were separated on agarose gel and densitometric analysis of the bands allowed semi-quantification. In the second group, iNOS and IL-1β were induced in hypothalamus, pituitary and liver, showing a peak at 3 h (p < 0.001), returning to baseline levels at 24 h. Neuronal NOS was not expressed in the liver under basal conditions or after LPS; in the hypothalamus and pituitary, nNOS was expressed basally but there was no change after LPS. In the first group, iNOS and IL-1β were again induced in all three tissues studied, but with a delayed time course compared to the second and third groups; the peak change for IL-1β occurred at 8 h (p < 0.05), again returning to baseline levels at 24 h. The peak for iNOS occurred at 24 h. HO₁ and HO₂ were expressed in all three tissues under basal conditions; HO₁ was increased at 1 h in the liver in the second group, and at 3 h in the pituitary in the third group. There was no change in either HO₁ or HO₂ in the hypothalamus at any dose at any time point. We conclude that IL-1β and iNOS are induced in rat hypothalamus and pituitary following various doses of endotoxin. We speculate that while IL-1β may mediate stimulation of the HPA by endotoxin, NO generation may be involved in the counter-regulation of this response.

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Section: Introductionsupporting

confidence: 75%

Endotoxin Induces Interleukin-1β and Nitric Oxide Synthase mRNA in Rat Hypothalamus and Pituitary

et al. 1998

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“…It should be noted that H 2 O 2 may block by itself the enzymatic activity of SOD1 [33], and therefore provoke the intracellular accumulation of O – 2 . Recent evidence also supports that SOD1 downregulation facilitates the reaction of the O – 2 in excess with NO [15], a situation that, in our model, would compromise the normal function of NO as inhibitory factor of neuropeptide release [22, 23, 34]. Consistent with this notion, the present study revealed that a deficit of O – 2 , caused by treating tissues with the SOD1 analogs Mn(III)-porphyrin [27]or TEMPOL [28], could actually reduce both basal and H 2 O 2 -stimulated AVP release.…”

Section: Discussionsupporting

confidence: 75%

“…Indeed, nNOS colocalizes with arginine vasopressin (AVP) and oxytocin in the rat hypothalamus [20, 21], and is also present in the nerve terminals of the neurohypophysis [19]. Furthermore, it has been shown that NO inhibits AVP release from rat-isolated hypothalami [22]and neurohypophysis [23]. Interestingly, this inhibitory effect of NO on neurosecretion is not mediated by cGMP, since the cell permeant cGMP analog 8-bromo-cGMP is unable to affect either basal or isoproterenol-stimulated AVP release from the rat neurohypophysis [24].…”

Section: Introductionmentioning

confidence: 99%

Oxidative Stress and a Murine Superoxide Dismutase-1 Mutation Promoting Amyotrophic Lateral Sclerosis Alter Neurosecretion in the Hypothalamo-Neurohypophyseal Axis

Lutz-Bucher¹,

Aguilar²,

Frydman³

et al. 1999

Neuroendocrinology

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In this study, we examined the effects of oxidative stress on a nitric oxide (NO)-regulated neuroendocrine function, the release of arginine vasopressin (AVP) by the hypothalamo-neurohypophyseal axis. Treatment of mouse-isolated hypothalami and neurointermediate lobes () with H₂O₂ increased AVP release. This effect was inhibited by copper-zinc superoxide dismutase-1 (SOD1) analogs. By measuring cGMP accumulation as an indicator of biologically active NO, we found that H₂O₂ treatment decreased cGMP formation in both hypothalami and . We have previously shown that NO inhibits AVP release by a cGMP-independent mechanism. Given that H₂O₂ stimulated AVP release, while it reduced cGMP production, our findings strongly suggest that oxidative damage affects neurosecretion by reducing NO availability. To test whether such a mechanism may operate under pathological conditions with pronounced oxidative stress, we compared neurosecretion in wild-type and transgenic mice carrying a mutated form of SOD1 associated with human familial amyotrophic lateral sclerosis. Reminiscent of the data obtained from H₂O₂-treated tissues, hypothalami and from SOD1 mutants displayed decreased cGMP accumulation and increased AVP release, compared with tissues from wild-type littermates. Since neuronal NO synthase expression was not modified, we conclude that the perturbed free radical metabolism associated with the SOD1 mutation is likely to trap NO, and thereby alter neurosecretion, a mechanism that can be exacerbated in specific physiopathological conditions.

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“…In the rat, it is well established that the generation of NO may induce marked neuroendocrine changes, and in particular NO has been shown to inhibit the release of vasopressin both in vitro and in vivo (6,7). Both excitatory and inhibitory effects of NO generation have been shown on CRH release in vitro, but recent in vivo data again suggest a predominant inhibitory modula¬ tion (11).…”

Section: Discussionmentioning

confidence: 99%

“…These hypothalamic nuclei are the major source of corticotrophin-releasing factor (CRH) and vasopressin. Nitric oxide has been shown to inhibit stimulated CRH and vasopressin release in rats (6,7), but data in humans are few. Furthermore, while L-arginine is an established stimulus to growth hor¬ mone (GH) secretion in humans (8), it has not been established previously whether this effect is related to the generation of NO or not.…”

mentioning

confidence: 99%

l-Arginine is unlikely to exert neuroendocrine effects in humans via the generation of nitric oxide

Korbonits

Trainer

Fanciulli

et al. 1996

European Journal of Endocrinology

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There is now considerable evidence that nitric oxide is an important neuroregulatory agent, but there has been very little investigation of its possible role in neuroendocrine mechanisms in humans. We have investigated the effects of two nitric oxide precursors, L-arginine and molsidomine, under basal conditions on the pituitary hormones growth hormone (GH), prolactin, luteinizing hormone, follicle-stimulating hormone, thyrotrophin, adrenocorticotrophin (ACTH) and vasopressin, and also on serum cortisol; we have also studied the effect of L-arginine on circulating prolactin, ACTH and cortisol in normal human subjects under hypoglycaemic stress. L-Arginine stimulated both GH and prolactin release under basal conditions but had no effect on the other hormones studied, while the nitric oxide donor molsidomine showed no effect on any hormone studied. L-Arginine potentiated the hypoglycaemia-stimulated release of ACTH but did not influence the rise in GH. The current studies suggest that the effects of L-arginine on the stimulation of GH and prolactin release are unlikely to be mediated via the generation of nitric oxide.

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Nitric oxide modulates the release of vasopressin from rat hypothalamic explants.

Cited by 108 publications

References 0 publications

Endotoxin Induces Interleukin-1β and Nitric Oxide Synthase mRNA in Rat Hypothalamus and Pituitary

Endotoxin Induces Interleukin-1β and Nitric Oxide Synthase mRNA in Rat Hypothalamus and Pituitary

Oxidative Stress and a Murine Superoxide Dismutase-1 Mutation Promoting Amyotrophic Lateral Sclerosis Alter Neurosecretion in the Hypothalamo-Neurohypophyseal Axis

l-Arginine is unlikely to exert neuroendocrine effects in humans via the generation of nitric oxide

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