UNIPROT:P01178 - FACTA Search

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Query: UNIPROT:P01178 (oxytocin)
15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of NG-nitro-L-arginine methyl ester (NAME), a potent inhibitor of nitric oxide (NO) synthase, injected into different brain areas on penile erection and yawning induced by apomorphine or oxytocin was studied in male rats. The compound was found to be able to prevent the above behavioral responses dose dependently when injected into the paraventricular nucleus of the hypothalamus (PVN), but not in the caudate nucleus, medial septum, preoptic area, and the CA1 field of the hippocampus. When injected in the PVN, 5 micrograms of NAME induced a 30% reduction of apomorphine and oxytocin responses, while 20 micrograms induced an almost complete reduction. The effect of NAME seems to be related to the inhibition of guanylate cyclase secondary to the prevention of NO formation, because a dose-dependent reduction of apomorphine and oxytocin responses was obtained also with the inhibitor of guanylate cyclase methylene blue injected intracerebroventricularly (100-400 micrograms ICV), but not into the PVN. The results provide further support for a neurotransmitter role of central NO in the control of penile erection and yawning.
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PMID:Prevention by NG-nitro-L-arginine methyl ester of apomorphine- and oxytocin-induced penile erection and yawning: site of action in the brain. 793 38

Nitric oxide (NO), which was firstly identified as an endothelium-derived relaxing factor, has recently been demonstrated to be a neurotransmitter in the central and peripheral nervous systems. In the hypothalamus, abundant nitric oxide synthase (NOS) immunoreactivity and its histochemical marker, NADPH-diaphorase activity, have been demonstrated in the hypothalamo-neurohypophyseal system. In the present study, we examined whether NOS is coexpressed with posterior pituitary hormones in the rat hypothalamus by combination of oxytocin and vasopressin immunofluorescence and NADPH-diaphorase histochemistry. Most oxytocin-immunoreactive neurons in the paraventricular and supraoptic nuclei expressed NADPH-diaphorase activity, but virtually no vasopressin-immunoreactive neurons contained NADPH-diaphorase activity. This suggests that oxytocin neurons are the main source of NO production in the hypothalamic-pituitary system.
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PMID:Coexistence of oxytocin and NADPH-diaphorase in magnocellular neurons of the paraventricular and the supraoptic nuclei of the rat hypothalamus. 808 73

Nitric oxide (NO) synthase (NOS), the enzyme responsible for NO formation, is found in hypothalamic neurons containing oxytocin (OT), vasopressin (VP), and to a lesser extent corticotropin-releasing factor (CRF). Because NO is reported to modulate endocrine activity, we have investigated the hypothesis that endogenous NO participates in ACTH released by various secretagogues in the rat. In the adult male rat, the intravenous injection of interleukin-1 beta (IL-1 beta; 0.2-0.3 micrograms/kg), VP (0.3-0.9 micrograms/kg), and OT (30 micrograms/kg) significantly increased plasma ACTH and corticosterone levels. Pretreatment with the L-form, but not the D-form, of N omega nitro-L-arginine-methylester (L-NAME; a specific inhibitor of NOS) markedly augmented the effects of these secretagogues whether it was injected acutely or over a 4 d period. Blockade of NOS activity also caused significant (P < 0.01) extensions of the duration of action of IL-1 beta, VP, and OT. In contrast, L-NAME did not significantly alter the stimulatory action of peripherally injected CRF, or centrally administered IL-1 beta. Administration of L-arginine, but not D-arginine (100 mg/kg), used as a substrate for basal NO synthesis and which did not by itself alter the activity of the hypothalamic-pituitary-adrenal (HPA) axis, blunted IL-1-induced ACTH secretion, and reversed the interaction between L-NAME and IL-1 beta. The stimulatory action of endotoxin, a lipopolysaccharide that releases endogenous cytokines, was also augmented by inhibition of NO formation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:In the rat, endogenous nitric oxide modulates the response of the hypothalamic-pituitary-adrenal axis to interleukin-1 beta, vasopressin, and oxytocin. 815 53

Nitric oxide (NO), previously identified with endothelium derived relaxing factor (EDRF), is thought to play a role in central neurotransmission: it is characterized by high lipid solubility and short half life, and NO-synthase, the enzyme which generates NO from L-arginine, has been found in the central nervous system (CNS), both in neuronal and glial cells. NO is believed to be involved in many neural events, such as neurotoxicity from N-methyl-D-aspartate (NMDA) receptor overstimulation, brain damage from vascular stroke, fever, nociception, memory and appetite control. Recent evidence implicates NO as a modulator of endocrine secretions, with inhibition of insulin, growth hormone (GH) and oxytocin release and stimulation of vasopressin (AVP), adrenocorticotropin (ACTH) and corticotropin releasing hormone (CRH) release. NO and prostaglandins could mediate neuroendocrine activities of cytokines such as interleukin-1 (IL-1) and interleukin-2 (IL-2), particularly in the CNS.
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PMID:Nitric oxide: a gas as a modulator of neuroendocrine secretions. 818 Dec 9

We angiographically assessed the vasodilatory effects of vasopressin and oxytocin on the basilar arteries in dogs. Intracisternal bolus injections of vasopressin (100 pmol and 1 nmol) and oxytocin (1 and 10 nmol) produced dose-dependent increases in the internal diameter of the basilar arteries without affecting mean arterial blood pressure. The maximal dilatations of the basilar arteries induced by 1 nmol vasopressin and 10 nmol oxytocin were 142.3 +/- 19.9 and 136.8 +/- 25.5% of the baseline, respectively. When the same peptides were injected into the vertebral artery, the maximal dilatations were similar, but the duration of response was shorter. Pretreatment with intracisternal injection of 10 mumol NG-monomethyl-L-arginine (L-NMMA), which inhibits the synthesis of nitric oxide from L-arginine, suppressed the vasodilatory responses induced by intracisternal injection of vasopressin and oxytocin and by intraarterial injection of vasopressin. Calcitonin gene-related peptide also caused dilatation of the basilar artery when injected into the cisterna magna, but its effect was not blocked by L-NMMA. L-NMMA reduced the basal diameter of the basilar artery in a dose-dependent manner; L-arginine produced dose-dependent increases in diameter. The vasoconstriction induced by L-NMMA was reversed by high concentrations of L-arginine. These results suggest that vasopressin and oxytocin dilate the basilar arteries via the release of nitric oxide from both the intraluminal and the extraluminal sides and that synthesis and release of nitric oxide in the vascular wall contribute to maintenance of basal vascular tonus.
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PMID:Role of nitric oxide in the cerebral vasodilatory responses to vasopressin and oxytocin in dogs. 843 20

In order to investigate the mechanism of action by which oxytocin induces penile erection, the effect of NG-nitro-L-arginine methyl ester (NAME) and NG-monomethyl-L-arginine (NMMA), inhibitors of nitric oxide (NO) synthase, injected into the paraventricular nucleus of the hypothalamus (PVN) on the response to oxytocin injected into the PVN was studied in male rats. NAME and NMMA, but not NG-mono-methyl-D-arginine (D-NMMA), which does not inhibit NO-synthase, prevented in a dose-dependent manner the response to oxytocin. NAME was 4-5 times more potent than NMMA. NAME prevention of the oxytocin effect was not observed when NAME was given together with L-arginine but not with D-arginine. Oxytocin-induced penile erection was prevented by the oxytocin antagonist d(CH2)5Tyr(Me)-Orn8-vasotocin and by methylene blue, an inhibitor of guanylate cyclase, but not reduced hemoglobin, a NO scavenger, given intracerebroventricularly (i.c.v.). In contrast, both methylene blue and hemoglobin were ineffective when injected into the PVN, unlike d(CH2)5Tyr(Me)-Orn8-vasotocin. Penile erection was induced also by sodium nitroprusside and hydroxylamine, two NO donors, injected into the PVN. Like the oxytocin effect, the NO donor response was prevented by i.c.v. d(CH2)5Tyr(Me)-Orn8-vasotocin and methylene blue, but not hemoglobin. In contrast, the three compounds were ineffective in preventing the NO donor response when injected into the PVN. The present results suggest that oxytocin induces penile erection by activating NO synthase in the PVN. NO in turn activates oxytocinergic neurons projecting to extra-hypothalamic areas that control the expression of this male sexual function by a guanosine cyclic 3':5'-monophosphate (cGMP) independent mechanism at least in the PVN.
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PMID:Oxytocin-induced penile erection. Role of nitric oxide. 871 73

Nitric oxide (NO) is produced by the enzyme NO synthase (NOS) and may be involved in the regulation of nutrient and endocrine homeostasis via actions on neurones of the hypothalamic supraoptic (SON) and paraventricular (PVN) nuclei. The effects of water deprivation or food deprivation for 4 days on the abundance of messenger RNA encoding NOS in these nuclei in rats were examined using in situ hybridization. Water deprivation markedly increased the abundance of NOS mRNA in both the SON and PVN (225 +/- 11% of control, P < 0.05 and 261 +/- 34% of control, P < 0.01 respectively). NOS mRNA abundance also appeared to be increased in magnocellular accessory nuclei. Food deprivation decreased NOS mRNA abundance in the SON and PVN (42 +/- 6% and 52 +/- 7% of control respectively, both P < 0.05), while withdrawal of both food and water produced no significant net changes in the abundance of NOS mRNA. Treatment-induced alterations in NOS mRNA abundance were reflected by changes in NOS activity, as assessed by NADPH-diaphorase histochemistry, and NADPH-diaphorase staining was observed in neurones both positive and negative for oxytocin-like immunoreactivity. These findings suggest that NOS mRNA abundance, NOS enzymatic activity and presumably NO production are modulated in an activity-dependent manner in hypothalamic (magnocellular and parvocellular) neurones by alterations in fluid and nutrient homeostasis, and support data from other studies suggesting a role for NO in the central regulation of water and food intake in the rat.
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PMID:Food or water deprivation modulate nitric oxide synthase (NOS) activity and gene expression in rat hypothalamic neurones: correlation with neurosecretory activity? 880 71

The localization and distribution of nitric oxide synthase in the hypothalamus have been studied with an immunohistochemical technique using antibodies to neuronal rat nitric oxide synthase. Subsequent double-labeling experiments examined the colocalization patterns of nitric oxide synthase and several peptides. Our results demonstrate a widespread occurrence of nitric oxide synthase-immunoreactive nerve cell bodies and processes throughout the hypothalamus, especially in various parts of the preoptic region, in the supraoptic and paraventricular nuclei, the lateral hypothalamic area, the ventromedial and dorsomedial nuclei, the arcuate nucleus and various parts of the mammillary region. Double labeling experiments showed that nitric oxide synthase-like immunoreactivity coexists with substance P-like immunoreactivity in the medial preoptic area, with oxytocin-, cholecystokinin-and galanin message-associated peptide-like immunoreactivity in the supraoptic nucleus, with enkephalin, oxytocin- and corticotropin releasing factor-like immunoreactivity in the paraventricular nucleus and with enkephalin-like immunoreactivity in the arcuate nucleus. Furthermore, in the ventromedial nucleus, nitric oxide synthase-like immunoreactivity coexisted with enkephalin-, substance P-, and somatostatin-like immunoreactivity, and in the dorsomedial nucleus with enkephalin-, galanin message-associated peptide-and substance P-like immunoreactivity. In the mammillary region nitric oxide synthase-like immunoreactivity coexisted with enkephalin-, cholecystokinin-, and substance P-like immunoreactivity. Among these neuropeptides, enkephalin and substance P were most frequently found in nitric oxide synthase-immunoreactive neurons. We conclude that nitric oxide synthase-immunoreactive neurons contain neuropeptides in various parts of the hypothalamus, and that nitric oxide in the hypothalamus may be involved in a variety of neuroendocrine and autonomic functions.
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PMID:Immunohistochemical mapping of nitric oxide synthase in the rat hypothalamus and colocalization with neuropeptides. 881 20

Although milk yield of cows and goats is known to be closely related to the total flow of blood through the udder, a number of studies suggest that milk yield can vary independently. No studies have attempted to measure the proportion of total flow that is nutritive. Within the mammary gland, capillary networks form a basket-like architecture surrounding each alveolus. Notably, flow in individual capillaries is not constant and varies among capillaries. Capillary flow (measured by intravital microscopy) was decreased by oxytocin, which generally increased total flow in the mammary artery, suggesting that the proportion of total flow that is nutritive can vary. In addition to classic metabolic regulators (e.g., carbon dioxide and oxygen) of tissue blood flow, the mammary gland produces a number of vasodilatory compounds, including parathyroid hormone-related protein, insulin-like growth factor-I, prostacyclin, nitric oxide, and endothelin. All of these compounds have been shown to alter mammary blood flow. Mammary tissue also contains kallikrein and angiotensin-converting enzyme, which convert circulating kinins and angiotensin, respectively, into potent vasoactive compounds. A number of these compounds are produced by epithelial cells themselves, providing a mechanism for the functioning epithelium to control its own blood supply and, hence, nutrient flow for milk synthesis. In this review, we examine the nature of the mammary microcirculation, its behavior under different conditions, and some of the regulatory features of the mammary microvasculature.
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PMID:Regulation of blood flow in the mammary microvasculature. 887 13

1. The role of nitric oxide (NO) in the regulation of uterine contractility has yet to be clearly defined. We evaluated the effect of NO (in the form of S-nitroso-cysteine, CysNO) upon uterine contractility and guanosine 3',5'-cyclic monophosphate (cyclic GMP) accumulation in pregnant and nonpregnant guinea-pig myometrium. 2. While CysNO had no effect upon spontaneous contractile activity in either pregnant or nonpregnant uterine tissues, addition of CysNO resulted in an immediate and reversible relaxation of oxytocin- or acetylcholine (ACh)-evoked contractions. 3. Relaxation of agonist-evoked contractions in response to CysNO was associated with significant elevations in intracellular cyclic GMP concentrations ([cyclic GMP]i). 4. Elevations in [cyclic GMP]i were not required for relaxation, as inhibition of guanylyl cyclase by methylene blue prevented [cyclic GMP]i accumulation while having no effect upon the ability of CysNO to relax agonist-evoked contractions. 5. Addition of the cyclic GMP-analogues, 8-Br-cyclic GMP and PET-cyclic GMP, only at high concentrations, produced partial relaxation of agonist-contracted tissues, suggesting the possibility that cyclic GMP may be sufficient but not necessary for myometrial relaxation. 6. Our studies not only provide evidence for a functional role for NO-modulation of agonist-evoked contractions in the pregnant and nonpregnant guinea-pig uterus, but also that these occur by a mechanism which is not dependent upon guanylyl cyclase activity.
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PMID:Cyclic GMP-independent effects of nitric oxide on guinea-pig uterine contractility. 890 49

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