Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Because increased flow and shear stress upregulate endothelial (e) nitric oxide synthase (NOS) in adult endothelial cells in vivo and in vitro, we hypothesized that decreased pulmonary blood flow would decrease eNOS content in the late-gestation ovine fetus. To investigate the effects of decreased blood flow and the potential role of altered eNOS content in lung hypoplasia, we studied an animal model of lung hypoplasia after left pulmonary artery (LPA) ligation in nine fetal lambs (114-124 days gestation; term = 147 days). After at least 14 days, animals were killed, and lungs were harvested for histology, immunostaining, Western blot analysis for eNOS protein content, and biochemical assays of NOS activity. LPA ligation markedly reduced left lung size. Histology demonstrated loose connective tissue and airway immaturity in the left lungs. eNOS immunostaining demonstrated equal staining in the left pulmonary vessels compared with the right. Solitary endothelial cells staining for eNOS and factor VIII-related antigen were observed throughout the mesenchyme of left, but not right, lungs. eNOS protein content and activity were similar in left and right lungs. We conclude that, despite the absence of pulmonary blood flow and marked lung hypoplasia, eNOS content and NOS activity were not reduced after LPA ligation in the late fetal lung. We speculate that low pulmonary blood flow does not downregulate fetal pulmonary vascular eNOS expression and that other factors, such as paracrine or autocrine stimuli, may account for the persistence of eNOS in the developing lung circulation.
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PMID:Persistent eNOS in lung hypoplasia caused by left pulmonary artery ligation in the ovine fetus. 917 63

Vascular function changes following loss of ovarian hormones in women at menopause and in experimental animals following surgical ovariectomy. Little is known about changes in vascular function during hormonal transition from sexual immaturity (juvenile) to sexual maturity. Therefore, experiments were designed to determine effects of natural puberty on vascular function in female pigs. Tissue was studied from eight juvenile (2-3 mo) and eight adult (5-6 mo) female pigs. Plasma nitric oxide (NO) was measured, and mRNA for endothelium-derived NO synthase (eNOS) and eNOS protein were determined in aortic endothelial cells. Rings of coronary arteries were suspended for measurement of isometric force in organ chambers. Serum 17beta-estradiol levels were comparable in the two groups, whereas the arithmetic mean of progesterone levels was about two-thirds lower in adults compared with juvenile pigs. Plasma NO was significantly higher in juveniles compared with adults, but mRNA and protein for eNOS were comparable. In coronary arteries, an alpha2-adrenergic agonist caused greater endothelium-dependent relaxations in rings from juvenile compared with adult pigs. Relaxations to bradykinin were similar in arteries from both groups, but inhibition of NO reduced relaxations only in arteries from juvenile pigs. Relaxations from NO were greater in arteries from adult compared with juvenile female pigs. In conclusion, coronary arterial endothelial and smooth muscle responses are selectively modulated at puberty in female pigs. At maturity, plasma NO is reduced and sensitivity of the smooth muscle to exogenous NO is increased. Posttranscriptional regulation of eNOS protein may explain differences in NO bioavailability in juvenile pigs.
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PMID:Effect of puberty on coronary arteries from female pigs. 1279 29

Nitric oxide (NO) is a diffusible chemical messenger functionally linked to N-methyl-D-aspartate (NMDA) receptor activity and has been shown to be involved in modulating numerous pathways in the central nervous system. In order to investigate the role of the neuronal NO synthase type I (nNOS)/NO system in the postnatal development of dorsal horn nociceptive pathways in rats, the specific nNOS inhibitor 7-nitroindazole sodium salt (7-NI) and the non-specific NOS inhibitor nitro-L-arginine methyl ester (L-NAME) were applied spinally at postnatal days (P) 14, 21, 28 and >56 (adult) and their effects on neuronal responses were compared. In response to a train of 16 noxious electrical stimuli, the wide dynamic range neurones in the deep dorsal horn showed a dose-dependent inhibition of C-fibre-evoked response, post-discharge and windup to both 7-NI and L-NAME. No difference between any age group was observed with either agent on these responses. However, the effect of both 7-NI and L-NAME on the primary evoked response, a measure of the events occurring pre-synaptic and intrinsic to the neurone recorded, was significantly different between the P14 and older age groups. nNOS is known to be expressed later in postnatal development than the NMDA receptor and from the results presented here, it is fully mature and functional from P14 onwards. The subtle differences in attenuation of the primary evoked response at P14 compared with older ages may reflect the immaturity of the dorsal horn and in particular the incomplete development of intrinsic and descending inhibitory controls.
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PMID:Neuronal nitric oxide synthase modulation of dorsal horn neuronal responses in the rat: a developmental study. 1461 56

We report a newborn with fetal alcohol syndrome with severe feeding intolerance and failure to thrive due to pyloric stenosis. This illustrates the importance of early recognition of pyloric stenosis in fetal alcohol syndrome to improve nutrition and growth. We speculate that pyloric stenosis in neonates results from the absence or immaturity of intrinsic nitric oxide synthase-containing neurons in the pyloric muscle in children of alcohol-addicted mothers.
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PMID:Fetal alcohol syndrome and pyloric stenosis: alcohol induced or an association? 1591 53

The aim of the present study is to give a review of the postnatal development of peripheral chemoreceptors - carotid body, paraganglia, and pulmonary neuroendocrine cells (PNEC) - with implications in Sudden Infant Death Syndrome (SIDS). In the postnatal period, the hypoxic chemosensitivity of the carotid body gradually develops. Changes include proliferation of type I and II cells, increased numbers of dense core vesicles and K+ channels, and modifications of neurotransmitter/neuromodulator and receptor expression. Chromaffin paraganglia show increased expression of nitric oxide synthase and neuropeptides, and increased innervation. Innervation of PNEC develops fully only in the first postnatal period, after which their density falls. The neuropeptides produced by PNEC also changes, with increased expression of calcitonin gene-related peptide and neuropeptide YY and reduced expression of calcitonin and gastrin-releasing peptide. Most of the findings in the carotid body of SIDS victims, i.e., decrease in type I cells and dense cytoplasmic granules, and increase in progenitor cells, indicates immaturity of the carotid body, which may play a role in SIDS in the form of underlying biologic vulnerability. Aorticopulmonary paraganglia hyperplasia and increase of PNEC are also found in SIDS, and may be epiphenomena of alterations of the respiratory function with a pathogenetical role in SIDS. A comprehensive view of the pathogenesis of SIDS should also arise from the integration of peripheral chemoreceptors findings with neuro- and cardiopathologic ones.
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PMID:Peripheral chemoreceptors: postnatal development and cytochemical findings in Sudden Infant Death Syndrome. 1807 92