Role of K+ channels in the pathophysiology of primary aldosteronism

Hypertension

Volumn 59, Issue 3, 2012, Pages 534-536

  Carey, Robert M ^a  

^a UNIVERSITY OF VIRGINIA HEALTH SYSTEM   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

3(OR 17)BETA HYDROXYSTEROID DEHYDROGENASE; ALDOSTERONE; CALCIUM CHANNEL T TYPE; INWARDLY RECTIFYING POTASSIUM CHANNEL; POTASSIUM CHANNEL; RENIN; TWIK RELATED ACID SENSITIVE POTASSIUM CHANNEL 1; TWIK RELATED ACID SENSITIVE POTASSIUM CHANNEL 2; TWIK RELATED ACID SENSITIVE POTASSIUM CHANNEL 3; UNCLASSIFIED DRUG; VOLTAGE GATED CALCIUM CHANNEL;

ADRENALECTOMY; ALDOSTERONE BLOOD LEVEL; CALCIUM CELL LEVEL; ESSENTIAL HYPERTENSION; GENETIC ASSOCIATION; HUMAN; HYPERALDOSTERONISM; HYPERTENSION; HYPOKALEMIA; IDIOPATHIC DISEASE; METABOLIC ALKALOSIS; NONHUMAN; NOTE; PATHOPHYSIOLOGY; PLASMA RENIN ACTIVITY; PRIMARY HYPERALDOSTERONISM; PRIORITY JOURNAL; SINGLE NUCLEOTIDE POLYMORPHISM; SOMATIC MUTATION;

ADENOMA; ADRENAL GLAND NEOPLASMS; ALDOSTERONE; DNA, NEOPLASM; FEMALE; G PROTEIN-COUPLED INWARDLY-RECTIFYING POTASSIUM CHANNELS; GERM-LINE MUTATION; HUMANS; HYPERALDOSTERONISM; MALE;

EID: 84857624957     PISSN: 0194911X     EISSN: 15244563     Source Type: Journal    
DOI: 10.1161/HYPERTENSIONAHA.111.188060     Document Type: Note

References (7)

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