Studies on hyperkalemic periodic paralysis. Evidence of changes in plasma Na and Cl and induction of paralysis by adrenal glucocorticoids.

No abstract is available for this paper.

• Publication year

  1971

• Venue

  Journal of Clinical Investigation

• Publication date

  Unknown publication date

• Fields of study

  Medicine

• Identifiers
  DOI 10.1172/JCI106468PMID 4322666PMCID PMC291902
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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• Lower Ca2+ enhances the K+-induced force depression in normal and HyperKPP mouse muscles

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• The Potential of Modulating Na+ K+ Atpase Pumps and Katp Channels in the Development of a New Therapy to Treat Hyperkalemic Periodic Paralysis

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• Understanding the physiology of the asymptomatic diaphragm of the M1592V hyperkalemic periodic paralysis mouse

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• Contractile abnormalities of mouse muscles expressing hyperkalemic periodic paralysis mutant NaV1.4 channels do not correlate with Na+ influx or channel content.

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• Calcium Alleviates Symptoms in Hyperkalemic Periodic Paralysis by Reducing the Abnormal Sodium Influx

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• Lessons learned from muscle fatigue: implications for treatment of patients with hyperkalemic periodic paralysis.

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• Na+,K+-pump stimulation improves contractility in isolated muscles of mice with hyperkalemic periodic paralysis

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• Targeted mutation of mouse skeletal muscle sodium channel produces myotonia and potassium-sensitive weakness.

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• Clinical and ultrastructural observations in a kindred with normo-hyperkalaemic periodic paralysis.

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