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Pagina 1 a partire dal 345 risultati
[Role of the inositol phosphate cycle in the cardioprotective effect of adaptation to intermittent hypoxia].
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The impact of adaptation to intermittent hypoxia of different duration (for 20 and 40 days) on the inositol triphosphate-diacylglycerol (ITP-DAG) regulatory contour in the heart was investigated. For this, isolated heart alpha 1-adrenoreactivity to phenylephrine and phospholipase (PhL-C) activities
Enhanced inositol trisphosphate response to alpha 1-adrenergic stimulation in cardiac myocytes exposed to hypoxia.
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Myocardial ischemia elicits an enhanced responsivity to alpha 1-adrenergic stimulation and a reversible increase in alpha 1-adrenergic receptor number. In adult cardiac myocytes, alpha 1-adrenergic receptor number increases two- to threefold after 10 min of hypoxia, an increase similar to that seen
Effect of chronic hypoxia on alpha-1 adrenoceptor-mediated inositol 1,4,5-trisphosphate signaling in ovine uterine artery.
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The present study examined the effect of chronic hypoxia on coupling efficiency of alpha-1 adrenoceptors to inositol 1,4,5-trisphosphate (InsP3) signaling in ovine uterine artery. Chronic hypoxia did not change the time course of InsP3 formation, but significantly decreased the potency (pD2: 6.17
Inositol trisphosphate is involved in norepinephrine- but not in hypoxia-induced pulmonary arterial contraction.
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The role that second messengers play in pulmonary vasoconstriction is not understood. The purpose of this study was to directly measure inositol phosphates in isolated pulmonary arterial preparations before and during norepinephrine (NE) stimulation and acute hypoxia. Rat main pulmonary arteries
Hypoxia enhances cellular proliferation and inositol 1,4, 5-triphosphate generation in fibroblasts from bovine pulmonary artery but not from mesenteric artery.
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When pulmonary hypertension occurs in the face of hypoxia there is remodeling of all three layers of the pulmonary vessels, but in particular, there is an increase in number of adventitial fibroblasts. Hypoxia causes vasoconstriction in the pulmonary circulation and vasodilation in the systemic
Effects of in vitro hypoxia on depolarization-stimulated accumulation of inositol phosphates in synaptosomes.
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The effects of potassium and in vitro histotoxic hypoxia (i.e. KCN) on phosphatidylinositol turnover in rat cortical synaptosomes were determined. [2-3H] Inositol prelabelled rat synaptosomes were prepared from cerebral cortex slices that had been incubated with [2-3H] inositol. Depolarization with
Transient global brain hypoxia-ischemia in adult rats: neuronal damage, glial proliferation, and alterations in inositol phospholipid hydrolysis.
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A model of ischemic-hypoxic brain injury which combines bilateral occlusion of common carotid arteries for 10 min and mild hypoxia (15% O2 for 10 min before and during occlusion) was developed. Global ischemia was assessed by a simplified EEG recording indicating isoelectric line, i.e. full arrest
Fetal and placental cyclic inositol phosphohydrolase in normoxia and hypoxia.
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Cyclic inositol phosphohydrolase (cIPH) converts cyclic inositol monophosphate (cIP), a putative modulator of cell growth, into inositol monophosphate. We hypothesized that hypoxic-ischemic injury alters cIPH activity in the placenta. On the 29th day of gestation pregnant rabbits were randomized to
Hypoxia differently modulates gene expression of inositol 1,4,5-trisphosphate receptors in mouse kidney and HEK 293 cell line.
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Hypoxia is a state of insufficient oxygen supply of the tissue or cell. Kidney tissue is highly sensitive to oxygen deprivation and easily develops renal ischemic injury. Calcium transporters very sensitively react to oxygen deficiency. We investigated whether hypoxia affects the gene expression of
Inositol tetrakisphosphate (IP4)- and inositol triphosphate (IP3)-dependent Ca2+ influx in cortical neuronal nuclei of newborn piglets following graded hypoxia.
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Previous studies have shown that hypoxia results in a modification of the binding characteristics of the neuronal nuclear membrane inositol tetrakisphosphate (IP4) and inositol triphosphate (IP3) receptors. The present study tests the hypothesis that hypoxia-induced modification of the IP4 and IP3
Hypoxia-induced modification of the inositol triphosphate receptor in neuronal nuclei of newborn piglets: role of nitric oxide.
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Previous studies have shown that hypoxia results in increased Ca2+ influx in neuronal nuclei and generation of nitric oxide (NO) free radicals in the cerebral cortical tissue of newborn piglets. The present study tests the hypothesis that hypoxia results in modification of the inositol triphosphate
Functional Role of Intracellular Calcium Receptor Inositol 1,4,5-Trisphosphate Type 1 in Rat Hippocampus after Neonatal Anoxia.
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Anoxia is one of the most prevalent causes of neonatal morbidity and mortality, especially in preterm neonates, constituting an important public health problem due to permanent neurological sequelae observed in patients. Oxygen deprivation triggers a series of simultaneous cascades, culminating in
Suppression of hypoxia-induced HIF-1alpha and of angiogenesis in endothelial cells by myo-inositol trispyrophosphate-treated erythrocytes.
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Allosteric regulation of oxygen delivery by RBCs may have significant effects on tumor growth. Indeed, angiogenesis, the formation of new blood vessels, is induced in growing tumors by low oxygen partial pressure. Hypoxia-inducible genes are switched on, among which are the VEGF gene and its
Treatment of hypoxia-dependent cardiovascular diseases by myo-inositol trispyrophosphate (ITPP)-enhancement of oxygen delivery by red blood cells.
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Heart failure is a consequence of progression hypoxia-dependent tissue damages. Therapeutic approaches to restore and/or protect the healthy cardiac tissue have largely failed and remain a major challenge of regenerative medicine. The myo-inositol trispyrophosphate (ITPP) is a modifier of
Myo-inositol trispyrophosphate-mediated hypoxia reversion controls pancreatic cancer in rodents and enhances gemcitabine efficacy.
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Hypoxia and dysfunctional tumor vessels represent a prominent feature of pancreatic cancer, being, at least in part, responsible for chemotherapy resistance and immune suppression in these tumors. We tested whether the increase of oxygen delivery induced in vivo by myo-inositol trispyrophosphate
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