Activation of ENaC by AVP contributes to the urinary concentrating mechanism and dilution of plasma

American Journal of Physiology - Renal Physiology

Volumn 308, Issue 3, 2015, Pages F237-F243

  Mironova, Elena ^a   Chen, Yu ^b   Pao, Alan C ^b   Roos, Karl P ^c   Kohan, Donald E ^c   Bugaj, Vladislav ^a   Stockand, James D ^a  

^a UNIVERSITY OF TEXAS HEALTH SCIENCE CENTER AT SAN ANTONIO   (United States)

^b STANFORD UNIVERSITY SCHOOL OF MEDICINE   (United States)

^c UNIVERSITY OF UTAH HEALTH SCIENCES CENTER   (United States)

Author keywords

Aldosterone; Arginine vasopressin; Epithelial Na+ channel; Epithelial transport; Hypertension; Hyponatremia; Na+transport

Indexed keywords

ARGIPRESSIN; BENZAMIL; DESMOPRESSIN; EPITHELIAL SODIUM CHANNEL; HYPERTONIC SOLUTION; SODIUM CHLORIDE; SODIUM;

ADULT; ANIMAL EXPERIMENT; ANIMAL TISSUE; ARTICLE; BLOOD PRESSURE REGULATION; CONTROLLED STUDY; DILUTION; DISEASE EXACERBATION; FLUID BALANCE; HOMEOSTASIS; HYPERNATREMIA; KIDNEY CONCENTRATING CAPACITY; MALE; MICTURITION; MOUSE; NONHUMAN; PRIORITY JOURNAL; REGULATORY MECHANISM; RENIN ANGIOTENSIN ALDOSTERONE SYSTEM; SODIUM BLOOD LEVEL; SODIUM URINE LEVEL; URINE OSMOLALITY; ANIMAL; BLOOD; C57BL MOUSE; DISEASE MODEL; HYPONATREMIA; KIDNEY; METABOLISM; PHYSIOLOGY; URINE;

ANIMALS; ARGININE VASOPRESSIN; DISEASE MODELS, ANIMAL; EPITHELIAL SODIUM CHANNELS; HOMEOSTASIS; HYPERNATREMIA; HYPONATREMIA; KIDNEY; MICE, INBRED C57BL; RENIN-ANGIOTENSIN SYSTEM; SODIUM;

EID: 84922210649     PISSN: 1931857X     EISSN: 15221466     Source Type: Journal    
DOI: 10.1152/ajprenal.00246.2014     Document Type: Article

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