Genetic deletion of AT1a receptors attenuates intracellular accumulation of ANG II in the kidney of AT1a receptor-deficient mice

American Journal of Physiology - Renal Physiology

Volumn 293, Issue 2, 2007, Pages

  Li, Xiao C ^a   Navar, L Gabriel ^b   Shao, Yuan ^a   Zhuo, Jia L ^a,c  

^a HENRY FORD HOSPITAL   (United States)

^b WAYNE STATE UNIVERSITY SCHOOL OF MEDICINE   (United States)

^c TULANE UNIVERSITY HEALTH SCIENCES CENTER   (United States)

Author keywords

Kidney; Losartan; Receptor endocytosis; Urinary sodium excretion

Indexed keywords

ANGIOTENSIN 1A RECEPTOR; ANGIOTENSIN II; LOSARTAN; ANGIOTENSIN 1 RECEPTOR; ANGIOTENSIN RECEPTOR ANTAGONIST; POTASSIUM; SODIUM;

ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; BODY WEIGHT; CELL AGGREGATION; CONTROLLED STUDY; ENDOCYTOSIS; GENE DELETION; HYPERTENSION; MALE; MOUSE; NATRIURESIS; NONHUMAN; PRIORITY JOURNAL; PROTEIN AGGREGATION; SYSTOLIC BLOOD PRESSURE; ANIMAL; AUTORADIOGRAPHY; BLOOD PRESSURE; C57BL MOUSE; DRINKING; GENETICS; KIDNEY; METABOLISM; MOUSE MUTANT; PHYSIOLOGY; URINE;

ANGIOTENSIN II; ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKERS; ANIMALS; AUTORADIOGRAPHY; BLOOD PRESSURE; DRINKING; ENDOCYTOSIS; KIDNEY; LOSARTAN; MALE; MICE; MICE, INBRED C57BL; MICE, KNOCKOUT; POTASSIUM; RECEPTOR, ANGIOTENSIN, TYPE 1; SODIUM;

EID: 34548385407     PISSN: 1931857X     EISSN: 15221466     Source Type: Journal    
DOI: 10.1152/ajprenal.00489.2006     Document Type: Article

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