UNIPROT:P01185 - FACTA Search

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Query: UNIPROT:P01185 (vasopressin)
23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nitric oxide (NO) is known to be involved in the modulation of neuroendocrine function. To clarify the role of different isoforms of NO synthase (NOS) in the neuroendocrine response to immune challenge, the expressions of neuronal NOS (nNOS) and inducible NOS (iNOS) genes in the hypothalamus following lipopolysaccharide (LPS) injection were examined using in situ hybridization. NOS activity was also determined by NADPH-diaphorase (NADPH-d) histochemistry. LPS (25 mg/kg) or sterile saline was injected intraperitoneally to male Wistar rats and the rats sacrificed 30 min, or 1, 2, 3, 5, 12 or 24 h after injection. nNOS mRNA expression in the paraventricular nucleus (PVN) was significantly increased 2 h after LPS injection. iNOS mRNA, which was not detected until 2 h after LPS injection, was significantly increased in the PVN 3 h after LPS injection. Both RNA expressions had returned to basal levels by 12 h after LPS injection. The number of NADPH-d positive cells was significantly increased 5 h after LPS injection. iNOS expression was more robust in parvocellular PVN, while nNOS was distributed mainly in the magnocellular PVN. Double in situ hybridization histochemistry revealed that some of the iNOS- (48.4%) or nNOS-positive cells (34. 3%) in the parvocellular PVN expressed CRF mRNA. The results demonstrate that LPS-induced sepsis causes significant increases in nNOS and iNOS gene expression with different time-courses and distributions, and that iNOS mRNA was more frequently co-localized with CRF-producing parvocellular neurons in the PVN. Thus, NO produced by iNOS and nNOS may play an important role in the neuroendocrine response to an immune challenge. Distinct differences in the distribution and time-course changes of iNOS and nNOS suggest different roles for the hypothalamic-pituitary-adrenal axis and/or neurohypophyseal system.
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PMID:Distinct distribution and time-course changes in neuronal nitric oxide synthase and inducible NOS in the paraventricular nucleus following lipopolysaccharide injection. 1006 18

Hypothalamic nuclei close to the third ventricle (VIII) represent key structures in avian osmoregulation concerned with the control of salt gland activity and release of the antidiuretic hormone [Arg8]vasotocin (AVT). Nitric oxide (NO) acting as a paracrine transmitter in the hypothalamus has been shown to contribute to the maintenance of salt and fluid balance in mammals. The saltwater-acclimated duck was used in the present study as a well-characterized osmoregulatory model to investigate the role of central NO in hypothalamic perception or integration of osmoregulatory signals in marine birds. During osmotically induced steady-state salt gland secretion, the VIII of conscious ducks was microperfused with artificial cerebrospinal fluid (aCSF) alone, aCSF containing the NO-donor SNAP or the peptide [Val5]angiotensin II (ANGII) and alterations in salt gland activity, arterial pressure and the release of AVT were continuously monitored. No changes occurred during intracerebroventricular microperfusion with aCSF. Central application of ANGII, a known inhibitory hypothalamic transmitter in the control of salt gland function, markedly blocked salt gland osmolal excretion. Central stimulation with the NO-donor SNAP significantly reduced osmolal excretion from 0.41+/-0.02 to 0. 22+/-0.04 mosmol/min. Both ANGII and SNAP caused a rise in plasma AVT at either slightly elevated (ANGII) or constant (SNAP) arterial pressure. Employing NADPH-diaphorase histochemistry in the duck hypothalamus to localize sites of NO synthesis, periventricular neurons, nerve fibers in close association to the VIII and also parvocellular neurons of the paraventricular nucleus could be labeled. These data suggest a modulatory role for hypothalamic NO within the central osmoregulatory circuitry controlling salt gland function and AVT release in marine birds.
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PMID:Central action of nitric oxide in the saltwater-acclimated duck: modulation of extrarenal sodium excretion and vasotocin release. 1021 70

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 (NIL) 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 NIL. 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 NIL 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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PMID:Oxidative stress and a murine superoxide dismutase-1 mutation promoting amyotrophic lateral sclerosis alter neurosecretion in the hypothalamo-neurohypophyseal axis. 1034 79

The effect of inhibition of nitric oxide (NO) synthesis on the responses of blood pressure (BP), heart rate (HR), and renal sympathetic nerve activity (RSNA) during hemorrhaging was examined with the use of an NO synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), in conscious rats. In the 0.9% saline group, hemorrhage (10 ml/kg body wt) did not alter BP but significantly increased HR and RSNA by 88 +/- 12 beats/min and 67 +/- 12%, respectively. Intravenous infusion of L-NAME (50 microg. kg(-1). min(-1)) significantly attenuated these tachycardic and sympathoexcitatory responses to hemorrhage (14 +/- 7 beats/min and 26 +/- 12%, respectively). Pretreatment of L-arginine (87 mg/kg) recovered the attenuation of HR and RSNA responses induced by L-NAME (92 +/- 6 beats/min and 64 +/- 10%, respectively). L-NAME by itself did not alter the baroreceptor reflex control of HR and RSNA. Hemorrhage increased the plasma vasopressin concentration, and its increment in the L-NAME-treated group was significantly higher than that in the 0.9% saline group. Pretreatment with the vascular arginine vasopressin V(1)-receptor antagonist OPC-21268 (5 mg/kg) recovered the attenuation of RSNA response induced by L-NAME (54 +/- 7%). These results indicate that NO modulated HR and RSNA responses to hemorrhage but did not directly affect the baroreceptor reflex arch. It can be assumed that NO modulated the baroreflex function by altering the secretion of vasopressin induced by hemorrhage.
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PMID:Role of nitric oxide in regulation of renal sympathetic nerve activity during hemorrhage in conscious rats. 1040 75

The investigation was performed on the medial (MMS) and lateral (LMS) magnocellular subdivisions of the hypothalamic paraventricular nuclei (HPN). The histochemical activity NO synthesizing enzyme nitric oxide synthase or NOS whose histochemical marker is NADPH-diaphorase (NADPH-D), immunocytochemical content of oxytocin (OXY), vasopressin (VP) and nucleoli sizes (squares) were studied in the mature male rats under experimental reconstruction of the both micro- and macrogravity, which are factors of the gravity field changes acting to the body during the space flight. Two experimental effects were used: B--tail suspending (imitation of the microgravity effects), C--centrifugation at 2 G (imitation of the macrogravity effects). The effect durations were designed as a time period when body is mostly affected by (1 day) and adapted (15 days) to the stress. There were 6 animal groups. 1--B(15 days), 2--B(15 days) succeeded by C(1 day), 3--B(15 days) succeeded by C(15 days), 4--C(1 day), 5--C(15 days), 6--intact animals. The histochemically and immuno-cytochemically stained neurons developing the high, moderate and small reaction intensity were counted in serial HPN sections under the light microscope and the results obtained were transformed to percent neuron contents. The nucleoli squares were examined by using the TV analyser. The histochemical staining intensity of NADPH-D in MMS is enhanced in the animals of the groups 1-4; the number of NADPH-D staining neurons with high enzyme activity was increased in 8-14 times. In the animals of group 5 the NADPH-D activity did not differ from the intact animals. The number of MMS neurons with high OXY immunoreactivities was increased up to 1.5-1.7 times in groups 1-5 if compared to those of intact controls. VP-positive neurons of LMS developed the similar increase in number of the high staining neurons in experimental animals as well as OXY-positive neurons of MMS. The nucleoli enlargement was observed in MMS (in 1.3-1.5 times) of groups 1-5 (insignificantly in group 5) and in the most magnocellular neurons LMS (in 1.5-1.7 times) of group 2-5 except group 1 where nucleoli were insignificantly decreased. The nucleoli sizes of group 4 were more than group 5. So the hypothalamo-neurohypophyseal system was activated in the animals subjected of the earthly correlates of micro- and macrogravity. The data obtained suggest involvement both the nonconventional neurotransmitter NO and stress-related peptides OXY and VP in the mechanisms subserving adaptation to the extreme factors by what a human has to be faced with during the space flight.
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PMID:[The participation of the nontraditional neuromediator nitric oxide in the mechanisms of adaptation to extreme conditions]. 1042 Apr 74

This investigation describes the migration and emergence of significant numbers of what appear to be neuron-like cells upon the surface of the median eminence of the adult rodent neurohypophyseal system of the endocrine hypothalamus following the trauma of hypophysectomy. These cells appear to migrate through the neuropil of the underlying median eminence and emerge in large numbers upon the surface of the third cerebral ventricle within 7 days following hypophysectomy (axotomy) of supraoptic (SON) and paraventricular neurites (PVN) of the adult neurohypophyseal system. Previous investigations have demonstrated regeneration of the neural stem and neural lobe in a variety of mammalian species (Adams et al., J Comp Neurol, 1969;135:121-144; Beck et al., Neuroendocrinology, 1969;5:161-182; Scott et al., Exp Neurol, 1995;131-1:23-39; Scott and Hansen, Vir Med 1997;124:249-261). It also has been demonstrated that the process of regeneration is invariably accompanied by the up-regulation of nitric oxide synthase (NOS), the enzyme that catalyzes arginine to nitric oxide (NO) and that both neurohypophyseal regeneration, as well as migration and emergence of neuron-like cells upon the surface of the adjacent third cerebral ventricle, is associated with the up-regulation of NOS and increased expression of NO. It also has been amply demonstrated that this entire process of neurohypophyseal regeneration and cell migration is completely inhibited by the introduction of the antagonist of nitric oxide, namely, nitroarginine (Scott et al., Exp Neurol, 1995;131-1:23-39; Scott and Hansen, Vir Med, 1997;124:249-261). The emergence and migratory dynamics of this novel cell line upon the floor of the rodent third cerebral ventricle are discussed with respect to the role of the ubiquitous free radical NO and the implications and potential clinical applications of neuronal migration following trauma in the human central nervous system (CNS).
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PMID:Post-traumatic migration and emergence of a novel cell line upon the ependymal surface of the third cerebral ventricle in the adult mammalian brain. 1052 82

In the present study, we investigated the effects of a nitric oxide (NO) precursor, L-arginine, on the effect of different drugs, [trans-3, 4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)-cyclohexyl]-benzeneacetamid e hydrochloride] (U-50,488, a kappa-opioid receptor agonist); dPTyr(Me)AVP (a vasopressin receptor antagonist); dizocilpine (MK-801, a N-methyl-D-aspartate (NMDA) receptor antagonist), to block the development of morphine tolerance or NO release in Sprague-Dawley rat hippocampal slices (450 microm). Slices were continuously superfused with artificial cerebrospinal fluid (ACSF) or drugs at 1 ml/min. Nichrome wire electrodes were placed in the Schaffer-collateral pathway and used to deliver biphasic 0.2-ms pulses of 5-30 V (0.033 Hz). A glass microelectrode was placed in the CA1 area to record population spikes. The amount of NO released in the superfusate was measured as nitrite formation. When the slices were superfused with 10 microM morphine, the amplitude of population spikes increased 200%-300% in 30-40 min. However, this effect of morphine decreased, i.e., tolerance developed, after continuous superfusion of morphine for 2-6 h. On the other hand, the nitrite level was increased about 250% of the control level through 6 h of morphine superfusion. Co-superfusion of L-arginine with morphine could further increase the nitrite level and also facilitate the development of morphine tolerance. On the other hand, 3-Br-7-nitroindazole (a neuronal NO synthase inhibitor) decreased the nitrite level significantly and blocked the development of morphine tolerance. When either U-50,488 (200 nM) or dPTyr(Me)AVP (500 pM) or MK-801 (500 pM) was co-superfused with morphine (10 microM), the development of morphine tolerance was blocked significantly and the nitrite level decreased to 100%-150% of the control level. L-arginine (500 nM) significantly reversed the effect of these drugs to block the development of morphine tolerance or to decrease the nitrite level through 6 h of superfusion. These data suggest that NO may play a key role in the development of morphine tolerance. Drugs which suppress the synthesis or release of NO would be expected to block the development of morphine tolerance.
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PMID:The role of nitric oxide in the development of morphine tolerance in rat hippocampal slices. 1058 26

Magnocellular neurones in the supraoptic nucleus and paraventricular nucleus express mRNA for nitric oxide synthase (NOS) and the expression becomes more prominent when the release of vasopressin or oxytocin is stimulated. It has also been reported that NO donors inhibit the electrical activity of supraoptic nucleus neurones, but the mechanism involved in the inhibition remains unclear. In the present study, to know whether modulation of synaptic inputs into supraoptic neurones is involved in the inhibitory effect of NO, we measured spontaneous excitatory and inhibitory postsynaptic currents (EPSCs and IPSCs) from rat supraoptic nucleus neurones in slice preparations identified under a microscope using the whole-cell mode of the slice-patch-clamp technique. The NO donor, S-nitroso-N-acetylpenicillamine (SNAP), reversibly increased the frequency of spontaneous IPSCs mediated by GABAA receptors, without affecting the amplitude, indicating that NO potentiated IPSCs via a presynaptic mechanism. The NO scavenger, haemoglobin, suppressed the potentiation of IPSCs by SNAP. On the other hand, SNAP did not cause significant effects on EPSCs mediated by non-NMDA glutamate receptors. The membrane permeable analogue of cGMP, 8-bromo cGMP, caused a significant reduction in the frequency and amplitude of both IPSCs and EPSCs. The results suggest that NO preferentially potentiates the inhibitory synaptic inputs into supraoptic nucleus neurones by acting on GABA terminals in the supraoptic nucleus, possibly via a cGMP-independent mechanism. The potentiation may, at least in part, account for the inhibitory action of NO on the neural activity of supraoptic neurones.
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PMID:Preferential potentiation by nitric oxide of spontaneous inhibitory postsynaptic currents in rat supraoptic neurones. 1071 23

The renal vascular response to vasopressin and its modulation were evaluated in vivo by infusing the peptide directly into the renal artery of anaesthetized rats. The intra-renal artery (i.r.a) infusion of vasopressin induced a dose-dependent decrease in renal blood flow. Vasoconstriction was obvious at a dose of 3 ng/kg per min and reached a maximum at 100 ng/kg per min. The dose required for a half-maximal response (ED50) was 24+/-4 ng/kg per min (mean+/-SEM, n=8), corresponding to an estimated concentration in renal arterial blood required for a half-maximal response (EC50) of 1.9+/-0.6 nM. Thiobutabarbitone anaesthesia markedly increased plasma vasopressin concentration. This increase was prevented partially by hypotonic hydration of the rats without any change in the renal vascular response to exogenous vasopressin. Vasopressin-induced vasoconstriction dose/response curves were similar in homozygous and heterozygous Brattleboro rats. Infusion of desmopressin (1-1000 ng/kg per min, i.r.a.), a vasopressin V2 receptor-selective agonist, failed to induce renal vasodilation or vasoconstriction. In the presence of SR 49059 (1 mg/kg i.v.), a vasopressin V1A receptor antagonist that completely abolished the vasopressin-induced renal vasoconstriction, desmopressin again failed to induce vasodilation. Inhibition of nitric oxide synthase by N(omega)-nitro-L-arginine (L-NNA, 100 microg/kg for 10 min and 7.5 microg/kg per min, i.r.a.) enhanced vasopressin-induced renal vasoconstriction (EC50 0.6+/-0.1 nM, P<0.05). In contrast, cyclooxygenase blockade by indomethacin (5 mg/kg, i.v.) neither modified the vasopressin-induced decrease in renal blood flow nor altered the potentiation of vasoconstriction by L-NNA. These results show that the constrictor response of the rat renal vascular bed in vivo is observed only with high local concentrations of vasopressin. This hyporeactivity in vivo was not explained by an anaesthesia-elicited increase in endogenous vasopressin, nor by a modulatory effect linked to V2 receptor activation or prostanoid release. In contrast, NO release contributed to the attenuation of vasopressin-induced renal vasoconstriction.
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PMID:Nitric oxide, but not vasopressin V2 receptor-mediated vasodilation, modulates vasopressin-induced renal vasoconstriction in rats. 1073 Oct 46

Utilization of the acute and chronically instrumented Sprague-Dawley rat model has provided new and informative data about the mechanisms of, and the role that circulating arginine vasopressin plays in, the regulation of blood flow to the renal medulla. Regional changes of blood flow were measured using implanted optical fibres and laser-Doppler flowmetry techniques. Transcriptional and translational sites of the V1a and V2 receptors were determined in microdissected intrarenal vascular segments from the cortex and medulla. Results from acute and chronic studies indicate the following. First, physiological elevations of plasma vasopressin concentration seen with 48 h of water restriction reduce blood flow to the inner medulla (via V1 receptors) while maintaining a constancy of blood flow to the outer medulla. Reduction of medullary blood flow is necessary to optimize urine osmolality during water restriction. Second, increases of plasma vasopressin concentration of as little as 8 pg ml(-1), which produce no change in baseline arterial pressure or renal cortical blood flow, can lower medullary blood flow selectively and greatly attenuate the arterial pressure-blood flow and pressure-natriuresis relationship. Third, medullary blood flow does not remain reduced in the face of sustained elevations of plasma vasopressin concentration, which appears to be related to the inability of vasopressin to produce a sustained hypertension. Fourth, V1a receptor mRNA and protein are present in the isolated cortical and medullary vasculature, but the V2 receptor mRNA and protein are found only in tubular segments. Levels of V2 receptor mRNA during water restriction were quantified using a competitive RT-PCR and a deletion mutant RNA transcript to control for the efficiency of the reaction, and Western blot analysis was utilized for quantification of the V2 receptor protein. The results demonstrated a time-dependent downregulation of the V2 receptor mRNA and protein within the rat kidney, specifically in the outer medulla. Fifth, the vasopressin-induced vasoconstriction of the medullary vasa recta microvessels was shown to be mediated via V1a receptors, and this response is normally modulated by vasopressin-stimulated release of nitric oxide (NO), via extravascular (presumably medullary collecting duct ) stimulation of V2 receptors. Finally, chronic vasopressin administration (10 days) increased nitric oxide synthase activity in the outer medulla and interstitial NO concentration in the medulla. These changes are essential to provide a constancy of blood flow to the renal medulla and buffer against the hypertensive actions of this potent vasoconstrictor peptide.
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PMID:Control of the renal medullary circulation by vasopressin V1 and V2 receptors in the rat. 1079 26

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