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Arginine vasopressin mediates the chloroquine induced increase in renal sodium excretion
Author(s) -
Musabayane C. T.,
Windle R. J.,
Forsling M. L.,
Balment R. J.
Publication year - 1996
Publication title -
tropical medicine and international health
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.056
H-Index - 114
eISSN - 1365-3156
pISSN - 1360-2276
DOI - 10.1046/j.1365-3156.1996.d01-81.x
Subject(s) - arginine , vasopressin , chloroquine , endocrinology , medicine , excretion , pharmacology , sodium , chemistry , immunology , malaria , biochemistry , amino acid , organic chemistry
Summary We postulated that chloroquine increases plasma arginine vasopressin (AVP) concentrations thus altering renal Na + clearance. Therefore, we studied a relationship between plasma AVP concentrations and urinary Na + output in separate groups of Sprague‐Dawley (SD) rats administered chloroquine (3 μg/min) for 1h 20 min. We also monitored Na + excretion rates in Brattleboro AVP‐deficient Di rats challenged with hypotonic saline load and administered chloroquine for 1 h 20 min. To establish whether chloroquine‐induced changes in renal Na + excretion were mediated via AVP VT receptors, we studied Na + excretion rates in groups of SD rats administered chloroquine or AVP in the presence of AVP V, receptor antagonist (1‐(β‐mercapto‐(β,β‐cyclopentamethylenepropionic acid)‐2‐O‐methyltyrosine arginine vasopressin (d(CH 2 ) 5 (Tyr(Me) 2 ) AVP) at 11 pmol/min for 1 h 20 min. The Na + excretion rate rose significantly ( P <0.01) from a pretreatment level of 9.8 ± 1.0 μmol/min to a peak of 14.1 ± 0.9 μmol/min in SD rats ( n = 7) administered chloroquine. The Na + excretion rate remained unaltered around 8.5 μmol/min in rats simultaneously administered chloroquine and the AVP V 1 receptor antagonist. This compared with control rats (8.1 ± 0.5 μmol/min, n = 7) and animals administered AVP V 1 receptor antagonist alone (8.7 ± 0.6 μmol/min, n = 7). Chloroquine did not affect urine flow, Na + or K + excretion rates in Brattleboro AVP‐deficient Di rats. Administration of AVP alone was associated with significant increases in renal Na + excretion rate. Blockade of AVP V 1 receptors abolished the AVP‐dependent increase in urinary Na + loss. We conclude that at least part of the chloroquine‐induced increase in Na + excretion is mediated by chloroquine stimulating an increase in plasma AVP concentration.