Hypotonic saline infusion alters the renal response to amino acids
in man.
Appiani, Aldo Claris, Amedea S. Tirelli, Gianluigi Ardissino, Valeria
Dacco', Eugenia Moretto, Carlo Corbetta, Laura Guidi and Baroukh M.
Assael.
Department of Pediatrics, University of Milan, and *Pharmacy and
Laboratory of Istituti Clinici di Perfezionamento, Milan, Italy
APStracts 5:0179F, 1998.
We investigated the effects of hypotonic saline-induced modifications
of extracellular volume and sodium handling on the renal and
metabolic response to amino acids (AA). Renal hemodynamics (Inutest,
PAH clearance), plasma AA and glucagon levels, and urea and sodium
excretion were studied in seven adult volunteers infused for 2 h, on
six separate occasions, according to the following protocols: 1) high
AA solution (300 mg/min/1.73 m2); 2) low AA solution (150 mg/min/1.73
m2); 3) low AA + 2000 ml/1.73 m2 0.23% saline solution; 4) high AA +
0.23% saline; 5) high AA + 0.45% saline; 6) 0.45% saline alone. The
GFR rise induced by the high AA solution was similar to that induced
by the low AA solution (D GFR +24+/-6 and +20.2+/-7 ml/min/1.73 m2
respectively) whereas the plasma AA and glucagon levels and urea
excretion rate increases were related to AA dose. The addition of
0.23% saline to the low AA solution and of 0.45% saline to the high
AA solution blunted the renal hemodynamic response (D GFR +6.6+/-10.1
and +11.4+/-8.3 ml/min/1.73 m2 respectively) without modifying the
pattern of plasma AA and glucagon levels and urea excretion observed
with the AA infusion alone. Urinary sodium excretion increased from
baseline with each protocol, and rose even further when saline was
added to AA. A negative correlation (r=-0.38 p<0.05) was found
between the changes from basal values in GFR and those in sodium
excretion rate with high AA infusion at different levels of sodium
concentration. These data suggest that AA-induced hyperfiltration
might be blunted by hypotonic saline infusion, possibly through an
acute modification of renal sodium handling and extracellular volume.
Received 31 October 1997; accepted in final form 30 September
1998.
APS Manuscript Number F412-7.
Article publication pending Am. J. Physiol. (Renal Physiology).
ISSN 1080-4757 Copyright 1998 The American Physiological Society.
Published in APStracts on 20 October 1998