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diabetic neuropathies/kalium
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[The effects of hyperglycemia on axonal sodium and potassium currents in human diabetic neuropathy].
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Allodynia and hyperalgesia in diabetic rats are mediated by GABA and depletion of spinal potassium-chloride co-transporters.
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Diabetic rats show behavioral indices of painful neuropathy that may model the human condition. Hyperalgesia during the formalin test in diabetic rats is accompanied by the apparently paradoxical decrease in spinal release of excitatory neurotransmitters and increase in the inhibitory
Protective effects of hydrogen‑rich saline against experimental diabetic peripheral neuropathy via activation of the mitochondrial ATP‑sensitive potassium channel channels in rats.
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It has previously been demonstrated that hyperglycemia‑induced oxidative stress and inflammation are closely associated with the development of diabetic complications, including diabetic neuropathy. Additionally, mitochondrial ATP‑sensitive potassium (Mito‑K‑ATP) channels play a homeostatic role on
Cyclic adenosine 3',5'-monophosphate enhances sodium, potassium-adenosine triphosphatase activity in the sciatic nerve of streptozotocin-induced diabetic rats.
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We have investigated the relationship between cAMP and sodium,potassium-ATPase (Na+,K(+)-ATPase) activity in the sciatic nerves of rats treated with cilostazol, a potent phosphodiesterase inhibitor; iloprost, a stable prostacyclin analog; or (Bu)2cAMP, a cAMP analog, which increase cAMP content by
[Cellular mechanisms in diabetic neuropathy].
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Although the pathogenesis of distal diabetic neuropathy is still uncertain, a possible mechanism might be postulated on the basis of results of several experimental studies. Differences between animal and human models are obvious--especially with regard to the time factor, but in attempts at
Platelet sodium and potassium ATPase [corrected] activity and noradrenaline efflux rate in relation to autonomic and peripheral nerve function in insulin-dependent diabetic patients.
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Low sodium and potassium adenosine triphosphatase (ATPase) activity has been proposed as a mechanism behind diabetic neuropathy. In this study the platelet ATPase activity and platelet noradrenaline efflux rate were determined in 47 insulin-dependent diabetes mellitus (IDDM) patients and 20
Diabetes affects the expression of GABA and potassium chloride cotransporter in the spinal cord: a study in streptozotocin diabetic rats.
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Painful diabetic neuropathy is associated to hyperexcitability and spontaneous hyperactivity of spinal cord neurons. The underlying pathophysiological mechanisms are not clear. Increases in excitatory neurotransmission at the spinal cord, involving glutamate and SP, seem to account for the abnormal
[Some properties of mixed saliva in diabetic autonomic neuropathy].
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BACKGROUND
The purpose of this work was to determine the influence of diabetic autonomic neuropathy on some basic properties of saliva such as volume of stimulated mixed saliva, concentration and secretion rates of sodium, potassium and calcium ions, and of glucose.
METHODS
The study was carried out
Sodium-potassium-ATPase activity in the dorsal root ganglia of rats with streptozotocin-induced diabetes.
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Sodium-potassium-ATPase activity was measured in excised dorsal root ganglia of streptozotocin-diabetic rats, 2 months after induction of diabetes. In comparison with age-matched controls, there was a decrease in both the total and ouabain-insensitive activity, indicating an overall reduction in
[Pathogenesis and treatment of diabetic neuropathy].
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The pathogenesis of neuropathy and other late, degenerative complications of diabetes remains largely unresolved. Metabolic derangements thought to be responsible for their development are induced by chronic hyperglycaemia. The present studies concern as follows: sorbitol accumulation due to
Axonal potassium conductance and glycemic control in human diabetic nerves.
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OBJECTIVE
To investigate the effects of hyperglycemia on axonal excitability and potassium conductance in human diabetic nerves.
METHODS
Threshold tracking was used to measure excitability indices, which depend on potassium channels (supernormality, late subnormality, threshold electrotonus, and a
Gabapentin-induced rhabdomyolysis in a patient with diabetic neuropathy.
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Gabapentin (GBP) is a drug which is frequently used in diabetic neuropathy. Common adverse effects of GBP include drowsiness, dizziness, ataxia, somnolence, and fatigue. Rhabdomyolysis is an extremely rare side effect of GBP. In this report we describe a case of GBP-induced rhabdomyolysis in a
Gastrodin inhibits allodynia and hyperalgesia in painful diabetic neuropathy rats by decreasing excitability of nociceptive primary sensory neurons.
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Painful diabetic neuropathy (PDN) is a common complication of diabetes mellitus and adversely affects the patients' quality of life. Evidence has accumulated that PDN is associated with hyperexcitability of peripheral nociceptive primary sensory neurons. However, the precise cellular mechanism
Spinal Disinhibition in Experimental and Clinical Painful Diabetic Neuropathy.
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Impaired rate-dependent depression (RDD) of the Hoffman reflex is associated with reduced dorsal spinal cord potassium chloride cotransporter expression and impaired spinal γ-aminobutyric acid type A receptor function, indicative of spinal inhibitory dysfunction. We have investigated the
Reduction in voltage-gated K+ channel activity in primary sensory neurons in painful diabetic neuropathy: role of brain-derived neurotrophic factor.
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Abnormal hyperexcitability of primary sensory neurons plays an important role in neuropathic pain. Voltage-gated potassium (Kv) channels regulate neuronal excitability by affecting the resting membrane potential and influencing the repolarization and frequency of the action potential. In this study,
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