Endogenous central κ-opioid systems augment renal sympathetic nerve activity to maximally retain urinary sodium during hypotonic saline volume expansion

American Journal of Physiology - Regulatory Integrative and Comparative Physiology

Volumn 289, Issue 5 58-5, 2005, Pages

  Gottlieb, Helmut B ^a,b   Kapusta, Daniel R ^a  

^a LOUISIANA STATE UNIVERSITY SCHOOL OF MEDICINE   (United States)

^b University of Texas Health Science Center at San Antonio   (United States)

Author keywords

Antinatriuresis; Central nervous system; Endorphin; Nor binaltorphimine; Renal excretory function; Renal nerves; Sprague Dawley rats; Urinary sodium excretion; Urine flow rate

Indexed keywords

BINALTORPHIMINE; KAPPA OPIATE RECEPTOR; KAPPA OPIATE RECEPTOR ANTAGONIST; METHOHEXITAL;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; BODY WEIGHT; CARDIOVASCULAR RESPONSE; COMPUTER PROGRAM; CONSCIOUSNESS; CONTROLLED STUDY; DEVICE; DIURESIS; DRUG MECHANISM; KIDNEY FUNCTION; KIDNEY NERVE; MALE; NATRIURESIS; NONHUMAN; PRIORITY JOURNAL; RAT; SODIUM URINE LEVEL; URINARY EXCRETION; URINE FLOW RATE;

ANIMALS; HYPOTONIC SOLUTIONS; KIDNEY; MALE; NALTREXONE; NARCOTIC ANTAGONISTS; RATS; RATS, SPRAGUE-DAWLEY; RECEPTORS, OPIOID, KAPPA; SODIUM; SODIUM CHLORIDE; SYMPATHETIC NERVOUS SYSTEM; TIME FACTORS;

EID: 27144452571     PISSN: 03636119     EISSN: None     Source Type: Journal    
DOI: 10.1152/ajpregu.00302.2005     Document Type: Article

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