UMLS:C0406810 - FACTA Search

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Query: UMLS:C0406810 (NAME)
13,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Electrical field stimulation (4 Hz, 0.2 ms pulse duration, at a supramaximal voltage of 70 V, for 1 s) of isolated rat tail artery segments produced contraction which was lower in female than in male rats, and was reduced by streptozotocin-induced diabetes in both genders. This contraction was potentiated by vasopressin (10(-12)-10(-10) M) more in normoglycemic male than in normoglycemic female rats, and this effect of vasopressin was increased by the cyclooxigenase inhibitor meclofenamate (10(-5) M) in female control rats, but not in diabetic female, or control and diabetic male rats, and it was not modified by the nitric oxide synthase inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME, 10(-4) M). Endothelin-1 (10(-10)-3 x 10(-9) M) also potentiated the contraction to electrical stimulation. This potentiation was similar in all experimental groups, and it was not modified by meclofenamate or L-NAME. These results suggest that the potentiating effect of vasopressin, but not that of endothelin-1, on the sympathetic vasoconstriction, is lower in females than in males, probably by an increased release of vasodilating prostanoids, and this release may be reduced by diabetes in females.
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PMID:Diabetes abolishes the gender difference in vasopressin-mediated potentiation of sympathetic vasoconstriction. 1156 55

The effects of intracerebralventricular (icv) injection of nitric oxide (NO) donor and nitric oxide synthase (NOS) inhibitor on the spontaneous discharge of magnocellular neurons of paraventricular nucleus (PVN) of hypothalamus were investigated in urethane anaesthetized adult SD rats by using microelectrode extracellularly recording method. The results showed that icv injection of NO donor sodium nitroprusside (SNP) had dose-dependent inhibitory effects on vasopressin (VP) secreting units in PVN. Icv injection of NOS inhibitor N( )-nitro-L-arginine methyl ester (L-NAME) also inhibited all of the VP-secreting neurons examined. Both the drugs had no effect on almost all oxytocin (OT) secreting units. These results suggest that NO may differentially modulate the activities of OT and VP neurons.
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PMID:Effect of intracerebralventricular injection of nitric oxide donor and nitric oxide synthase inhibitor on the spontaneous discharge of magnocellular neurons of paraventricular nucleus in the rat. 1197 Nov 67

Magnocellular neurons are innervated by an excitatory histaminergic pathway. They also express neuronal NO synthase, interleukin-1beta (IL-1beta) and cyclo-oxygenase (COX). In normally hydrated rats when NO synthase activity is inhibited with N(G)-nitro-L-arginine methyl ester (L-NAME), administered intracerebroventricularly (i.c.v.), OT concentration in plasma increases. In the present study, the increase in hormone after L-NAME is attenuated by indomethacin, an inhibitor of COX, as well as by antagonists of histamine receptors at H1 (pyrilamine) and H2 (cimetidine) subtypes injected i.c.v. Moreover, enhanced OT secretion induced by centrally administered IL-1beta, but not naloxone (opiate receptor antagonist), is prevented by indomethacin. PGE2 and PGD2 (i.c.v.) stimulate OT release, but only PGD2 affects circulating vasopressin levels. Thus, NO inhibits release of OT stimulated by: (1) a COX-dependent mechanism, i.e. NO-->-(COX-->+PG-->+OT release); (2) histamine, i.e. NO-->-(histamine-->H1 and H2 receptors-->+OT release); and possibly (3) IL-1beta, i.e. NO-->-(IL-1beta-->+COX-->+PG-->+OT release). These interactions of NO, cytokine and histamine may be important for management of stress-induced activation of neuroendocrine systems.
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PMID:Nitric oxide, interleukin and prostaglandin interactions affecting the magnocellular system. 1202 Aug 69

The central nervous system plays an important role in the control of renal sodium excretion. We present here a brief review of physiologic regulation of hydromineral balance and discuss recent results from our laboratory that focus on the participation of nitrergic, vasopressinergic, and oxytocinergic systems in the regulation of water and sodium excretion under different salt intake and hypertonic blood volume expansion (BVE) conditions. High sodium intake induced a significant increase in nitric oxide synthase (NOS) activity in the medial basal hypothalamus and neural lobe, while a low sodium diet decreased NOS activity in the neural lobe, suggesting that central NOS is involved in the control of sodium balance. An increase in plasma concentrations in vasopressin (AVP), oxytocin (OT), atrial natriuretic peptide (ANP), and nitrate after hypertonic BVE was also demonstrated. The central inhibition of NOS by L-NAME caused a decrease in plasma AVP and no change in plasma OT or ANP levels after BVE. These data indicate that the increase in AVP release after hypertonic BVE depends on nitric oxide production. In contrast, the pattern of OT secretion was similar to that of ANP secretion, supporting the view that OT is a neuromodulator of ANP secretion during hypertonic BVE. Thus, neurohypophyseal hormones and ANP are secreted under hypertonic BVE in order to correct the changes induced in blood volume and osmolality, and the secretion of AVP in this particular situation depends on NOS activity.
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PMID:Nitrergic modulation of vasopressin, oxytocin and atrial natriuretic peptide secretion in response to sodium intake and hypertonic blood volume expansion. 1221 82

Inter-neuronal coupling is a relatively recently documented property of a wide variety of cell groups in the mammalian central nervous system. For many of these groups there is evidence that the coupling can be modulated by synaptic inputs. Incidence of dye coupling among vasopressin (VP) neurons of the rat supraoptic nucleus (SON) has been shown to increase in response to either activation of histamine H(1)-receptors or to increased NO production. Both of these effects involve activation of cGMP-dependent pathways. We tested the hypothesis that activation of H(1)-receptors resulted in downstream activation of NO synthase, which then mediated the H(1)-receptor effects. Putative VP neurons were intracellularly recorded and dye-injected in horizontal slices of hypothalamus, in which monosynaptic connections from the tuberomammillary nucleus (TM) were intact and electrically stimulated. Single-pulse TM stimulation evoked EPSPs and repetitive stimulation resulted in a nearly 3-fold increase in coupling incidence over unstimulated slices. TM-stimulated increased coupling was completely blocked by inhibitors of NO synthase (L-NAME) or of soluble guanylyl cyclase (ODQ or methylene blue), or pyrilamine, suggesting that the H(1)-receptor is not directly linked to guanylyl cyclase. Addition of the NO precursor, L-arginine or the NO donor, SNP, in combination with TM stimulation produced increases in coupling that were not significantly larger than those seen with stimulation alone, supporting the idea that a common pathway was used. We conclude that H(1)-receptors activate NO synthase via G-protein-coupled pathways and that NO working though its receptor, induces the downstream cGMP-dependent processes that result in increased inter-neuronal coupling.
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PMID:Histamine H1-receptor modulation of inter-neuronal coupling among vasopressinergic neurons depends on nitric oxide synthase activation. 1241 27

We have previously reported that chloroquine administration increases plasma vasopressin concentration and urinary sodium excretion in Sprague-Dawley rats. Because chloroquine has also been shown to stimulate nitric oxide production, the aim of this study was to determine whether nitric oxide mediates chloroquine-induced changes in renal function and secretion of vasopressin. Sprague-Dawley rats (n = 6-8/group) were infused with 2.5% dextrose under Intraval anesthesia (100 mg kg(-1) i.p.). After 3-h equilibration and a control hour, animals received either vehicle, chloroquine (0.04 mg h(-1)), N(omega)-nitro-L-arginine methyl ester (L-NAME) (nitric-oxide synthase inhibitor, 60 microg kg(-1) h(-1)), or combined chloroquine and L-NAME over the next hour. L-NAME or vehicle infusion continued for a further recovery hour. Plasma was collected from a parallel group of animals for vasopressin radioimmunoassay. Chloroquine stimulated a significant increase (p < 0.05) in urine flow rate, glomerular filtration rate, and sodium excretion over the hour of infusion, in comparison with vehicle-infused rats. These effects continued after cessation of chloroquine, reaching maxima in the following recovery hour. Coadministration of L-NAME abolished these effects, returning all parameters to levels comparable with those in vehicle-infused animals. Chloroquine administration was accompanied by a significant increase (p < 0.05) in plasma vasopressin, which was also reversed by L-NAME. The effects of chloroquine on renal function and vasopressin secretion seem to be mediated by pathways involving nitric oxide. These data suggest that chloroquine may stimulate nitric-oxide synthase both centrally, stimulating vasopressin secretion, and within the kidney, where it modulates glomerular hemodynamics and tubular function.
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PMID:The effect of chloroquine on renal function and vasopressin secretion: a nitric oxide-dependent effect. 1249 May 86

The isometric response to vasopressin of 2-mm-long segments of basilar, coronary, renal and tail arteries from male and female, control (normoglycemic) and streptozotocin-induced diabetic rats was studied. Vasopressin (10(-12)-3 x 10(-8) M) produced arterial concentration-dependent contraction, with a lower potency in coronary arteries from female than from male rats, and was similar for both genders in basilar, renal and tail arteries. This contraction was reduced by diabetes in basilar and coronary arteries, increased in renal arteries, and not modified in tail arteries, in both genders. Inhibition of nitric oxide synthesis with N(W)-nitro-L-arginine methyl ester (L-NAME, 10(-4) M) increased the contraction to vasopressin in coronary arteries from control female and diabetic female rats; as well as in renal arteries from control male and control female rats, but not in any other experimental group. Inhibition of cyclooxygenase with meclofenamate (10(-5) M) reduced the contraction to vasopressin in basilar arteries from diabetic female rats and in renal arteries from diabetic male rats, but not in any other experimental group. These results suggest that the response to vasopressin (a) has lower potency in female coronary arteries due to higher nitric oxide production; (b) is reduced by diabetes in basilar and coronary arteries from both genders, by mechanisms independent of nitric oxide and prostanoids; and (c) is increased by diabetes in renal arteries due to reduced production of nitric oxide in females, and to both reduced production of nitric oxide and increased production of prostanoids in males. Therefore, the effects of diabetes on vascular reactivity to vasopressin may differ between vascular beds, and the mechanisms underlay these effects may be distinct between genders.
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PMID:Vascular reactivity to vasopressin during diabetes: gender and regional differences. 1252 53

Nitric oxide (NO) is known to regulate the release of arginine-vasopressin (AVP) and oxytocin (OT) by the paraventricular nucleus (PVN) and the supraoptic nucleus (SON). The aim of the current study was to identify in these nuclei the NO-producing neurons and the NO-receptive cells in mice. The determination of NO-synthesizing neurons was performed by double immunohistochemistry for the neuronal form of NO synthase (NOS), and AVP or OT. Besides, we visualized the NO-receptive cells by detecting cyclic GMP (cGMP), the major second messenger for NO, by immunohistochemistry on hypothalamus slices. Neuronal NOS was exclusively colocalized with OT in the PVN and the SON, suggesting that NO is mainly synthesized by oxytocinergic neurons in mice. By contrast, cGMP was not observed in magnocellular neurons, but in GABA-, tyrosine hydroxylase- and glutamate-positive fibers, as well as in GFAP-stained cells. The cGMP-immunostaining was abolished by incubating brain slices with a NOS inhibitor (L-NAME). Consequently, we provide the first evidence that NO could regulate the release of AVP and OT indirectly by modulating the activity of the main afferents to magnocellular neurons rather than by acting directly on magnocellular neurons. Moreover, both the NADPH-diaphorase activity and the mean intensity of cGMP-immunofluorescence were increased in monoamine oxidase A knock-out mice (Tg8) compared to control mice (C3H) in both nuclei. This suggests that monoamines could enhance the production of NO, contributing by this way to the fine regulation of AVP and OT release and synthesis.
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PMID:The effects of nitric oxide on magnocellular neurons could involve multiple indirect cyclic GMP-dependent pathways. 1258 Nov 64

The antimalaria drug chloroquine is often taken against a background of analgesic nephropathy caused by nonsteroidal anti-inflammatory drugs such as paracetamol (acetaminophen). Chloroquine has marked effects on the normal kidney and stimulates an increase in plasma vasopressin via nitric oxide. The aim of this study was to determine the renal action of chloroquine in a model of analgesic nephropathy. Sprague-Dawley rats (n = 6-8/group) were treated with paracetamol (500 mg kg(-1) day(-1)) for 30 days in drinking water to induce analgesic nephropathy; control rats received normal tap water. Under intraval anesthesia (100 mg kg(-1)) rats were infused with 2.5% dextrose for 3 h to equilibrate and after a control hour they received either vehicle, chloroquine (0.04 mg h(-1)), N(omega)-nitro-L-arginine methyl ester (L-NAME, nitric-oxide synthase inhibitor, 60 micro g kg(-1) h(-1)) or combined chloroquine and L-NAME over the next hour. Plasma was collected from a parallel group of animals for vasopressin radioimmunoassay. Long-term paracetamol treatment resulted in a decrease in glomerular filtration rate (p < 0.05), sodium excretion (p < 0.001), and urine osmolality (p < 0.001), but no change in urine flow rate compared with untreated animals. Chloroquine administration in paracetamol treated rats induced a significant reduction (p < 0.05) in urine flow rate and a significant increase in plasma vasopressin (p < 0.001). These effects were blocked by coadministration of L-NAME and thus seem to be mediated by a pathway involving nitric oxide. However, these responses contrast with the chloroquine-induced diuresis previously observed in untreated rats, possibly reflecting paracetamol inhibition of renal prostaglandin synthesis and consequent moderation of vasopressin's action.
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PMID:Renal function in a rat model of analgesic nephropathy: effect of chloroquine. 1264 60

This work examines the role of nitric oxide (NO) in the periphery (i.e., on the pituitary) and the brain (particularly on corticotropin-releasing factor [CRF] and vasopressin [VP] neurons in the paraventricular nucleus [PVN] of the hypothalamus) as a modulator of the ACTH response to lipopolysaccharide. We previously showed that NO restricted the pituitary response to VP while it facilitated the synthesis of PVN CRF and VP. In our experience, only relatively high doses of lipopolysaccharide (>50 microg/kg, injected intravenously [i.v.]) cause detectable increases in PVN neuronal activation. Our hypothesis, therefore, was that pituitary NO-VP interactions would predominate in rats injected with a low dose of lipopolysaccharide (0.5 microg/kg, i.v.) while the stimulatory influence of the gas on PVN neuronal activity would play an important role following i.v. injection of a large dose of lipopolysaccharide (50 microg/kg, i.v.). We observed that the ability of 0.5 microg/kg lipopolysaccharide to release ACTH was significantly enhanced by the subcutaneous (s.c.), but not the intracerebroventricular (i.c.v.) injection of L-NAME, an arginine derivative that blocks NO synthesis. The effect of s.c. L-NAME was reversed by immunoneutralization of endogenous VP, which indicated that in this model, the ability of lipopolysaccharide to release ACTH depended, at least in part, on the influence exerted by NO on the pituitary response to VP. In rats injected with the high lipopolysaccharide dose, the s.c. injection of L-NAME decreased plasma ACTH levels compared to those in rats pretreated with the vehicle. The effect of s.c. L-NAME was not significantly altered by VP antibodies. These results indicate that in this model, the primary influence of NO was exerted in the PVN and/or its afferents and that it did not depend on a peripheral, VP-mediated effect of the gas. On the one hand, these data are at odds with our finding that the i.c.v. injection of L-NAME only marginally altered the ACTH response to the large dose of lipopolysaccharide. As i.c.v. injected L-NAME should have primarily decreased hypothalamic, but not pituitary NOS, its only modest influence on ACTH release may have been due to a balance between stimulating and inhibiting effects of NO within the brain. As high doses of lipopolysaccharide increase brain levels of prostaglandin, monoamine, and proinflammatory cytokines, it will be important to investigate the influence exerted by NO on these secretagogues and on their interactions with PVN CRF and VP neurons, which may help us resolve the issues raised by our results. Collectively, these data support our hypothesis that the mechanisms mediating the ACTH response to a low lipopolysaccharide concentration involve the inhibitory VP-mediated influence of NO on pituitary activity. By contrast, the stimulatory effect of high doses of lipopolysaccharide on ACTH release depends, at least in part, on the ability of NO to upregulate PVN neuronal activity.
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PMID:Role of nitric oxide in regulating the rat hypothalamic-pituitary-adrenal axis response to endotoxemia. 1279 48

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