guanosine/hypoxia

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Anoxia inhibits guanosine salvage in cardiac myocytes.

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The adult heart depends largely on salvage synthesis to supply its 5'-nucleotide needs. Previous work from this laboratory established that guanosine is metabolized into guanine 5'-nucleotides in heart cells, but that salvage rates are very slow as compared to adenosine. The author hypothesized that

Cyclic 3',5'-guanosine monophosphate-dependent protein kinase inhibits colon cancer cell adaptation to hypoxia.

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BACKGROUND Type 1 cyclic 3',5'-guanosine monophosphate-dependent protein kinase (PKG) has recently been reported to inhibit tumor growth and angiogenesis. These effects suggest that PKG activation may have therapeutic value for colon cancer treatment, but the signaling downstream of this enzyme is

Inhibition of Hypoxia-Inducible Factor 1 Alpha Accumulation by Glyceryl Trinitrate and Cyclic Guanosine Monophosphate.

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A key mechanism mediating cellular adaptive responses to hypoxia involves the activity of hypoxia-inducible factor 1 (HIF-1), a transcription factor composed of HIF-1α and HIF-1β subunits. The classical mechanism of regulation of HIF-1 activity involves destabilisation of HIF-1a via oxygen-dependent

Importance of schedule of administration in the therapeutic efficacy of guanosine: early intervention after injury enhances glutamate uptake in model of hypoxia-ischemia.

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Perinatal cerebral hypoxia-ischemia (HI) is an important cause of mortality and neurological disabilities such as cerebral palsy, epilepsy, and mental retardation. The potential for neuroprotection in HI can be achieved mainly during the recovery period. In previous work, we demonstrated that

Inosine and guanosine preserve neuronal and glial cell viability in mouse spinal cord cultures during chemical hypoxia.

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Murine spinal cord primary mixed cultures were treated with the respiratory inhibitor, rotenone, to mimic hypoxic conditions. Under these conditions neurons rapidly underwent oncosis (necrosis) with a complete loss in viability occurring within 260 min; however, astrocytes, which accounted for most

P2Y2 receptor up-regulation induced by guanosine or UTP in rat brain cultured astrocytes.

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Among P2 metabotropic ATP receptors, P2Y2 subtype seems to be peculiar as its upregulation triggers important biological events in different cells types. In non-stimulated cells including astrocytes, P2Y2 receptors are usually expressed at levels lower than P2Y1 sites, however the promoter region of

Atrial natriuretic peptide increases cyclic guanosine monophosphate immunoreactivity in the carotid body.

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The mammalian carotid body is a peripheral arterial chemoreceptor organ involved in the regulation of respiration, and in the modulation of blood pressure through reflex control of peripheral vascular resistance and cardiac output. In addition to its responsiveness to blood gases, the organ is also

Myocardial dysfunction and potential cardiac hypoxia in rats induced by carbon monoxide inhalation.

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BACKGROUND Results from both animal and human being studies provide evidence that inhalation of concentrations of carbon monoxide (CO) at around 100 ppm has antiinflammatory effects. These low levels of CO are incriminated in ischemic heart diseases experienced by cigarette smokers and, in some

Cicletanine blunts the pulmonary pressor response to acute hypoxia in rats.

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Cicletanine (CIC) recently has been shown to lower systemic arterial pressure in hypertensive animals and man by a mechanism that may involve potentiation of the vasodilator effect of atrial natriuretic peptide (ANP). We previously have shown that ANP prevents acute hypoxia-induced pulmonary

Effects of dimethylarginine dimethylaminohydrolase-1 overexpression on the response of the pulmonary vasculature to hypoxia.

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Acute and sustained hypoxic pulmonary vasoconstriction (HPV), as well as chronic pulmonary hypertension (PH), is modulated by nitric oxide (NO). NO synthesis can be decreased by asymmetric dimethylarginine (ADMA), which is degraded by dimethylarginine dimethylaminohydrolase-1 (DDAH1). We

Evidence that epithelium-dependent relaxation of vascular smooth muscle detected by co-axial bioassays is not attributable to hypoxia.

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1. The present study was undertaken to examine further the contribution of hypoxia to airway epithelium-dependent relaxation of rat aorta in the co-axial bioassay. 2. Endothelium-denuded rat aorta contracted with phenylephrine (0.05 microM) relaxed in a time-dependent manner (t1/2 = 8.3 +/- 0.4 min,

Role of neuronal NO synthase in relationship between NO and opioids in hypoxia-induced pial artery dilation.

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Nitric oxide (NO) contributes to hypoxia-induced pial artery dilation, at least in part, via the formation of guanosine 3',5'-cyclic monophosphate (cGMP) and subsequent release of Met-enkephalin and Leu-enkephalin in the newborn pig. In separate studies, these opioids were also observed to elicit

Role of activation of calcium-sensitive K+ channels in NO- and hypoxia-induced pial artery vasodilation.

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It has been previously observed that nitric oxide (NO) contributes to hypoxic pial artery dilation and that both sodium nitroprusside (SNP), a releaser of NO, and hypoxia elicit dilation via activation of ATP-sensitive K+ channels in the newborn pig. Other studies, however, have shown that NO

Effect of chronic hypoxia on K+ channels: regulation in human pulmonary vascular smooth muscle cells.

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We investigated the effects of chronic hypoxia on the major outward K+ currents in early cultured human main pulmonary arterial smooth muscle cells (HPSMC). Unitary currents were measured from inside-out, outside-out, and cell-attached patches of HPSMC. Chronic hypoxia depolarized resting membrane

cGMP prevents delayed relaxation at reoxygenation after brief hypoxia in isolated cardiac myocytes.

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Previous studies in isolated cardiac myocytes suggest that impaired relaxation during reoxygenation after brief hypoxia results from abnormal Ca(2+)-myofilament interaction. Recent studies indicate that guanosine 3',5'-cyclic monophosphate (cGMP)-elevating interventions selectively enhance

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