PS: Pain and sodium channels

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Sodium channels and pain

Although it is well established that hyperexcitability andyor increased baseline sensitivity of primary sensory neurons can lead to abnormal burst activity associated with pain, the underlying molecular mechanisms are not fully understood. Early studies demonstrated that, after injury to their axons, neurons can display changes in excitability, suggesting increased sodium channel expression, an...

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Voltage-gated sodium channels: therapeutic targets for pain.

OBJECTIVE To provide an overview of the role of voltage-gated sodium channels in pathophysiology of acquired and inherited pain states, and of recent developments that validate these channels as therapeutic targets for treating chronic pain. BACKGROUND Neuropathic and inflammatory pain conditions are major medical needs worldwide with only partial or low efficacy treatment options currently a...

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The role of sodium channels in neuropathic pain.

Our knowledge of the ion channels, receptors and signalling mechanisms involved in pain pathophysiology, and which specific channels play a role in subtypes of pain such as neuropathic and inflammatory pain, has expanded considerably in recent years. It is now clear that in the neuropathic state the expression of certain channels is modified, and that these changes underlie the plasticity of re...

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Epithelial sodium channels and hypertension.

Hypertension is a major risk factor for heart attacks, stroke, and kidney failure. It is estimated to cause as many as 25% of all deaths in the United States, particularly for African Americans, in whom the disease is both more common and more severe. Essential hypertension is a multifactorial disorder influenced by both genetic and environmental factors. Physiological studies have shown that t...

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Salt, sodium channels, and SGK1.

The hormone aldosterone increases extracellular fluid volume and blood pressure by activating epithelial Na+ channels (ENaCs). Serum- and glucocorticoid-induced kinase 1 (SGK1) is an aldosterone-stimulated signaling molecule that enhances distal nephron Na+ transport, in part by preventing the internalization of ENaCs from the plasma membrane. In this issue of the JCI, Zhang et al. demonstrate ...

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ژورنال

عنوان ژورنال: Clinical Genetics

سال: 2012

ISSN: 0009-9163

DOI: 10.1111/j.1399-0004.2012.01945.x