Changes in NADPH‐d Staining in the Paraventricular and Supraoptic Nuclei During Pregnancy and Lactation in Rats: Role of Ovarian Steroids and Oxytocin

Popeski, Naomi; Amir, Shimon; Woodside, Barbara

doi:10.1046/j.1365-2826.1999.00291.x

Cited by 41 publications

(42 citation statements)

References 63 publications

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“…This is the first study to show that this febrile response can be restored and that brain NO plays a determining role in the mechanism of fever suppression. This NO-mediated mechanism is consistent with previous reports that the expression of NOS within the brain is increased during late pregnancy (38,47,48) and that central NO donors can inhibit LPS-induced fever (21). The dose of L-NMMA that we used did not cause significant hyperthermia by itself in either day 19 and 20 pregnant, day 15 pregnant, or virgin female rats, demonstrating that the febrile response in near-term dams was due to a restoration of the neuroimmune response to LPS and not a nonspecific response to L-NMMA.…”

Section: Discussionsupporting

confidence: 93%

“…However, these increases can be blocked by the nonspecific COX inhibitor indomethacin (31, 44), indicating interactions between COX and NO activity. Oestrogen and progesterone, secreted during pregnancy, increase expression of endothelial NOS within cerebral blood vessels (33), and the neuronal NOS isoform is also increased in the hypothalamus during the late stages of pregnancy (38,47,48).There is growing evidence that NO is involved in thermoregulation through neural signaling (31,42). Neurons containing NOS have been identified in the medial preoptic area (3), a key integrative site for thermoregulatory signals.…”

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Suppression of endotoxin-induced fever in near-term pregnant rats is mediated by brain nitric oxide

Begg¹,

Kent²,

Mathai³

2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Begg DP, Kent S, McKinley MJ, Mathai ML. Suppression of endotoxin-induced fever in near-term pregnant rats is mediated by brain nitric oxide. Am J Physiol Regul Integr Comp Physiol 292: 2174-2178, 2007. First published March 1, 2007; doi:10.1152/ajpregu.00032.2007.-Over the last three decades, experiments in several mammalian species have shown that the febrile response to bacterial endotoxin is attenuated late in pregnancy. More recent evidence has established that the expression of nitric oxide synthase (NOS) enzymes is increased in the brain late in pregnancy. The current study investigated the possible role of brain nitric oxide in mediating the phenomenon of fever suppression. Core body temperature (T b) of near-term pregnant rats (day 19 and 20) was measured following inhibition of brain NOS and intraperitoneal injection of LPS (50 g/kg); they were compared with both day 15 pregnant and virgin animals. Intracerebroventricular injection with an inhibitor of NOS, N G -monomethyl-L-arginine citrate (L-NMMA; 280 g), in near-term pregnant rats restored the febrile response to LPS. As expected, near-term dams that received intracerebroventricular vehicle ϩ IP LPS did not increase T b, in contrast to the 1.0 Ϯ 0.2°C rise in Tb in dams treated with ICV L-NMMA ϩ IP LPS (P Ͻ 0.01). In virgin females and day 15 pregnant controls receiving this treatment, the increases in T b were 1.5 Ϯ 0.3°C and 1.6 Ϯ 0.4°C, respectively. Thus, blockade of brain NOS restored the febrile response to LPS in near-term dams; at 5 h postinjection, T b was 60 -70% of that observed in virgins and day 15 pregnant animals. Intracerebroventricular L-NMMA alone did not induce a significant change in Tb in any group. These results suggest that the mechanism underlying the suppression of the febrile response in near-term pregnancy is mediated by nitric oxide signaling in the brain. nitric oxide synthase; N G -monomethyl-L-arginine citrate; lipopolysaccharide; core body temperature; thermoregulation FEVER IS A REGULATED INCREASE in core body temperature (T b ) caused by initiation of heat-conserving and heat-producing systems. It plays a crucial role in the physiological response to infection by pathogens, improving the efficiency of lymphocytes and reducing the replication of many microorganisms (23). Fever can be caused by a number of different stimuli, such as infection with bacteria and viruses (27) or by stress (13,17). It has been widely documented that these factors result in the release of proinflammatory cytokines from macrophages (11). This results in the stimulation of central and peripheral cyclooxygenase (COX) enzymes that catalyze the synthesis of PGs (10). The enzymes COX-1 and COX-2 are the ratelimiting step in the production of PGs, and inhibition of COX blocks the febrile response (39). PGE 2 has been seen traditionally as the final step in the process of fever generation. The febrile response is integral to the body's defense against infection; however, if T b becomes excessively high, it endangers the host, as these temperatu...

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Section: Discussionsupporting

confidence: 93%

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confidence: 99%

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confidence: 99%

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Suppression of endotoxin-induced fever in near-term pregnant rats is mediated by brain nitric oxide

Begg¹,

Kent²,

Mathai³

2007

American Journal of Physiology-Regulatory, Integrative and Comp

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“…At this time, plasma progesterone levels would likely be elevated above that of nonpregnant rats. In contrast, in pregnant rats on the day of parturition after progesterone falls and is low or in rats where progesterone is withdrawn after hormone treatment to mimic the time of parturition, nNOS activity in both the SON and PVN is increased (38,53). Together, these data suggest that decreased nNOS expression in the PVN during pregnancy may be attributed to high progesterone levels rather than high estrogen levels.…”

Section: Discussionmentioning

confidence: 86%

Protective actions of estrogen on angiotensin II-induced hypertension: role of central nitric oxide

Xue¹,

Singh²,

Guo³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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.-The present study tested the hypotheses that 1) nitric oxide (NO) is involved in attenuated responses to ANG II in female mice, and 2) there is differential expression of neuronal NO synthase (nNOS) in the subfornical organ (SFO) and paraventricular nucleus (PVN) in response to systemic infusions of ANG II in males vs. females. Aortic blood pressure (BP) was measured in conscious mice with telemetry im-), an inhibitor of NOS, was administrated into the lateral cerebral ventricle for 14 days before and during ANG II pump implantation. Central infusion of L-NAME augmented the pressor effects of systemic ANG II in females (⌬21.5 Ϯ 2.2 vs. ⌬9.2 Ϯ 1.5 mmHg) but not in males (⌬29.4 Ϯ 2.5 vs. ⌬30.1 Ϯ 2.5 mmHg). Central administration of, a selective nNOS inhibitor, also significantly potentiated the increase in BP induced by ANG II in females (⌬17.5 Ϯ 3.2 vs. ⌬9.2 Ϯ 1.5 mmHg). In gonadectomized mice, central L-NAME infusion did not affect the pressor response to ANG II in either males or females. Ganglionic blockade after ANG II infusion resulted in a greater reduction in BP in central L-NAME-or L-VNIO-treated females compared with control females. Western blot analysis of nNOS protein expression indicated that levels were ϳ12-fold higher in both the SFO and PVN of intact females compared with those in intact males. Seven days of ANG II treatment resulted in a further increase in nNOS protein expression only in intact females (PVN, to ϳ51-fold). Immunohistochemical studies revealed colocalization of nNOS and estrogen receptors in the SFO and PVN. These results suggest that NO attenuates the increase in BP induced by ANG II through reduced sympathetic outflow in females and that increased nNOS protein expression associated with the presence of female sex hormones plays a protective role against ANG II-induced hypertension in female mice. sex hormone; nitric oxide/nitric oxide synthase; blood pressure NITRIC OXIDE (NO) and angiotensin II (ANG II) are important agents that regulate arterial blood pressure (BP). Vasoconstriction produced by sympathoexcitatory effects contributes to ANG II-induced pressor responses (13, 17). Conversely, NO has a hypotensive action via vasodilation and sympathoinhibition (36, 39). It has been shown that interactions between ANG II and NO occur in a variety of tissues, including the central nervous system (CNS) (40, 58). For example, microinjection of either an NO synthase (NOS) inhibitor or ANG II into the lateral ventricle or the paraventricular nucleus (PVN) increases the discharge of renal sympathetic nerves and elevates arterial BP and heart rate (HR) (25, 28, 52). Central or peripheral blockade of NOS potentiates or prolongs the pressor response to ANG II (9, 31). Conversely, overexpression of neuronal NOS (nNOS) within the PVN by adenoviral gene transfer significantly attenuates ANG II pressor responses (28).There is evidence from human and animal studies that hypertension is delayed and attenuated in females compared with males (11). Previous studies from our laboratory (54) have sh...

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“…It has been reported that physiological stimuli, such as pregnancy and lactation, could increase NOS expression in HNS. These activity-dependent enhancements never lead to neuronal death in HNS [36,37]. Taken together, it seems that enhanced NOS/NO induced by physiological stimuli or pathological stimulation of axonal injury may not cause neuronal death.…”

Section: Discussionmentioning

confidence: 90%

The Potential Role of Nitric Oxide Synthase in Survival and Regeneration of Magnocellular Neurons of Hypothalamo-Neurohypophyseal System

Yuan

Scott

et al. 2009

Neurochem Res

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Previous investigations from this laboratory have demonstrated that hypophysectomy induces up-regulation of neuronal nitric oxide synthase (nNOS) in magnocellular neurons of the mammalian hypothalamo-neurohypophyseal system (HNS). Accompanied by this upregulation of nNOS, both neuronal regeneration and degeneration are also observed in this system following hypophysectomy. The specific aim of this study was to determine the potential role of nNOS upregulation in neuronal survival and regeneration after hypophysectomy in the adult Sprague-Dawley (SD) rat by using a competitive nitric oxide synthase blocker, N(G)-nitrol-L: -arginine methyl ester (L: -NAME). We found that L: -NAME treatment effectively blocked the regeneration of magnocellular neurons of the rodent hypothalamus as observed in the lumen of the third cerebral ventricle following hypophysectomy. However, L: -NAME had no effect on the survival of magnocellular neurons in the supraoptic (SON) and paraventricular (PVN) nuclei after hypophysectomy. These results suggest that the induced increase of nNOS expression enhance the regenerative ability of magnocellular neurons of the HNS following hypophysectomy.

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Changes in NADPH‐d Staining in the Paraventricular and Supraoptic Nuclei During Pregnancy and Lactation in Rats: Role of Ovarian Steroids and Oxytocin

Cited by 41 publications

References 63 publications

Suppression of endotoxin-induced fever in near-term pregnant rats is mediated by brain nitric oxide

Suppression of endotoxin-induced fever in near-term pregnant rats is mediated by brain nitric oxide

Protective actions of estrogen on angiotensin II-induced hypertension: role of central nitric oxide

The Potential Role of Nitric Oxide Synthase in Survival and Regeneration of Magnocellular Neurons of Hypothalamo-Neurohypophyseal System

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