anandamide/hypoxia

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Endocannabinoid anandamide mediates hypoxic pulmonary vasoconstriction.

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Endocannabinoids are important regulators of organ homeostasis. Although their role in systemic vasculature has been extensively studied, their impact on pulmonary vessels remains less clear. Herein, we show that the endocannabinoid anandamide (AEA) is a key mediator of hypoxic pulmonary

Hypoxia training improves hepatic steatosis partly by downregulation of CB1 receptor in obese mice.

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Hypoxia training (HT) can reduce body weight and improve fatty liver. However, the mechanism is not clear. A previous study indicated that HT-induced weight loss might be associated with the endocannabinoid system (ECS), which has also been reported recently to be involved in the persistent lipid

ATP release from vascular endothelia occurs across Cx43 hemichannels and is attenuated during hypoxia.

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BACKGROUND Extracellular ATP is an important signaling molecule for vascular adaptation to limited oxygen availability (hypoxia). Here, we pursued the contribution of vascular endothelia to extracellular ATP release under hypoxic conditions. UNASSIGNED We gained first insight from studying ATP

Endocannabinoids and endocannabinoid-like compounds modulate hypoxia-induced permeability in CaCo-2 cells via CB1, TRPV1, and PPARα.

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We have previously reported that endocannabinoids modulate permeability in Caco-2 cells under inflammatory conditions and hypothesised in the present study that endocannabinoids could also modulate permeability in ischemia/reperfusion.

EXPERIMENTAL

The ALIAmide palmitoylethanolamide and cannabinoids, but not anandamide, are protective in a delayed postglutamate paradigm of excitotoxic death in cerebellar granule neurons.
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The amino acid L-glutamate is a neurotransmitter that mediates fast neuronal excitation in a majority of synapses in the central nervous system. Glutamate stimulates both N-methyl-D-aspartate (NMDA) and non-NMDA receptors. While activation of NMDA receptors has been implicated in a variety of

CB2 receptor-mediated effects of pro-inflammatory macrophages influence survival of cardiomyocytes.
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OBJECTIVE The endocannabinoid system and cannabinoid receptor 2 (CB2 receptor) have been associated with modulation of inflammatory response and myocardial adaptation after ischemic injury. In order to elucidate CB2 receptor-related effects during cellular interactions, we investigated cardiomyocyte

Endogenous cannabinoids are candidates for lipid mediators of bone cement implantation syndrome.
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Acute hypotension, hypoxemia, cardiac arrhythmias, cardiac arrest, (or a combination of these), and sudden death are well-recognized complications of the cemented hip arthroplasty procedure. Collectively, these are known as the bone cement implantation syndrome (BCIS). The endogenous cannabinoids,

Endocannabinoids protect cerebral cortical neurons from in vitro ischemia in rats.
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The endogenous cannabinoids (endocannabinoids) anandamide and 2-arachidonylglycerol increased cell viability in cerebral cortical neuron cultures subjected to 8 h of hypoxia and glucose deprivation. This effect was observed at nanomolar concentrations, was reproduced by a non-hydrolyzable analog of

System-specific O2 sensitivity of the tandem pore domain K+ channel TASK-1.
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Hypoxic inhibition of TASK-1, a tandem pore domain background K+ channel, provides a critical link between reduced O2 levels and physiological responses in various cell types. Here, we examined the expression and O2 sensitivity of TASK-1 in immortalized adrenomedullary chromaffin (MAH) cells. In

TASK-1 channels in oligodendrocytes: a role in ischemia mediated disruption.
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Oligodendrocytes are the myelinating cells of the CNS and, like neurons, are highly sensitive to ischemic damage. However, the mechanisms underlying cytotoxicity in oligodendrocytes during hypoxic/ischemic episodes are not fully understood. TASK-1 is a K(+) leak channel that mediates hypoxic

Protective role of the novel hybrid 3,5-dipalmitoyl-nifedipine in a cardiomyoblast culture subjected to simulated ischemia/reperfusion.
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This work investigated the acute effects of the calcium channel blocker nifedipine and its new fatty hybrid derived from palmitic acid, 3,5-dipalmitoyl-nifedipine, compared to endocannabinoid anandamide during the process of inducing ischemia and reperfusion in cardiomyoblast H9c2 heart cells. The

Pituitary adenylate cyclase-activating polypeptide (PACAP) stimulates the oxygen sensing type I (glomus) cells of rat carotid bodies via reduction of a background TASK-like K+ current.
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Pituitary adenylate cyclase-activating polypeptide (PACAP)-deficient mice are prone to sudden neonatal death and have reduced respiratory response to hypoxia. Here we found that PACAP-38 elevated cytosolic [Ca(2+)] ([Ca(2+)](i)) in the oxygen sensing type I cells but not the glial-like type II

An act of balance: Interaction of central and peripheral chemosensitivity with inflammatory and anti-inflammatory factors in obstructive sleep apnoea.
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OBJECTIVES

Central and peripheral chemosensitivity i.e. ventilatory response to CO₂ and O₂ are thought to be decisive for ventilatory control instability in obstructive sleep apnoea (OSA). Obesity is associated with chronic low level inflammation. Whether

Acid-sensing ion channels contribute to transduction of extracellular acidosis in rat carotid body glomus cells.
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Carotid body chemoreceptors sense hypoxemia, hypercapnia, and acidosis and play an important role in cardiorespiratory regulation. The molecular mechanism of pH sensing by chemoreceptors is not clear, although it has been proposed to be mediated by a drop in intracellular pH of carotid body glomus

Molecular pathogenesis of alcohol-induced hepatic fibrosis.
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Alcohol abuse is a main cause of liver fibrosis and cirrhosis in the western world. Although the major mechanisms of fibrogenesis are independent of the origin of liver injury, alcoholic liver fibrosis features distinctive characteristics, including the pronounced inflammatory response of immune

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anandamide/hypoxia

Endocannabinoid anandamide mediates hypoxic pulmonary vasoconstriction.

Hypoxia training improves hepatic steatosis partly by downregulation of CB1 receptor in obese mice.

ATP release from vascular endothelia occurs across Cx43 hemichannels and is attenuated during hypoxia.

Endocannabinoids and endocannabinoid-like compounds modulate hypoxia-induced permeability in CaCo-2 cells via CB1, TRPV1, and PPARα.

The ALIAmide palmitoylethanolamide and cannabinoids, but not anandamide, are protective in a delayed postglutamate paradigm of excitotoxic death in cerebellar granule neurons.

CB2 receptor-mediated effects of pro-inflammatory macrophages influence survival of cardiomyocytes.

Endogenous cannabinoids are candidates for lipid mediators of bone cement implantation syndrome.

Endocannabinoids protect cerebral cortical neurons from in vitro ischemia in rats.

System-specific O2 sensitivity of the tandem pore domain K+ channel TASK-1.

TASK-1 channels in oligodendrocytes: a role in ischemia mediated disruption.

Protective role of the novel hybrid 3,5-dipalmitoyl-nifedipine in a cardiomyoblast culture subjected to simulated ischemia/reperfusion.

Pituitary adenylate cyclase-activating polypeptide (PACAP) stimulates the oxygen sensing type I (glomus) cells of rat carotid bodies via reduction of a background TASK-like K+ current.

An act of balance: Interaction of central and peripheral chemosensitivity with inflammatory and anti-inflammatory factors in obstructive sleep apnoea.

Acid-sensing ion channels contribute to transduction of extracellular acidosis in rat carotid body glomus cells.

Molecular pathogenesis of alcohol-induced hepatic fibrosis.

Baz done ki pi konplè remèd fèy medsin te apiye nan syans