Hypotonic saline infusion alters the renal response to amino acids in men

Aldo Claris-Appiani, Amedea S. Tirelli, Gianluigi Ardissino, Valeria Daccò, Eugenia Moretto, Carlo Corbetta, Laura Guidi, Baroukh M. Assael

Research output: Contribution to journalArticle

Abstract

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, p-aminohippurate clearance), plasma AA, and glucagon levels, as well as 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 · 1.73 m-2); 2) low-AA solution (150 mg · min-1 · 1.73 m-2); 3) low AA + 2,000 ml/1.73 m2 of 0.23% saline solution; 4) high AA + 0.23% saline; 5) high AA + 0.45% saline; and 6) 0.45% saline alone. The glomerular filtration rate (GFR) rise induced by the high-AA solution was similar to that induced by the low-AA solution (ΔGFR = +24 ± 6 and +20.2 ± 7 ml · min-1 · 1.73 m-2, 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 (ΔGFR = +6.6 ± 10.1 and +11.4 ± 8.3 ml · min-1 · 1.73 m-2, 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 he blunted by hypotonic saline infusion, possibly through an acute modification of renal sodium handling and extracellular volume.

Original languageEnglish
JournalAmerican Journal of Physiology - Renal Physiology
Volume276
Issue number1 45-1
Publication statusPublished - Jan 1999

Fingerprint

Kidney
Amino Acids
Sodium
Glomerular Filtration Rate
Glucagon
Urea
Sodium Chloride
Hemodynamics
p-Aminohippuric Acid
Volunteers

Keywords

  • Glucagon
  • Renal hemodynamics
  • Sodium handling
  • Urea excretion

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

Hypotonic saline infusion alters the renal response to amino acids in men. / Claris-Appiani, Aldo; Tirelli, Amedea S.; Ardissino, Gianluigi; Daccò, Valeria; Moretto, Eugenia; Corbetta, Carlo; Guidi, Laura; Assael, Baroukh M.

In: American Journal of Physiology - Renal Physiology, Vol. 276, No. 1 45-1, 01.1999.

Research output: Contribution to journalArticle

Claris-Appiani, Aldo ; Tirelli, Amedea S. ; Ardissino, Gianluigi ; Daccò, Valeria ; Moretto, Eugenia ; Corbetta, Carlo ; Guidi, Laura ; Assael, Baroukh M. / Hypotonic saline infusion alters the renal response to amino acids in men. In: American Journal of Physiology - Renal Physiology. 1999 ; Vol. 276, No. 1 45-1.
@article{5ffd9bb511f544318a1047ebdece8a03,
title = "Hypotonic saline infusion alters the renal response to amino acids in men",
abstract = "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, p-aminohippurate clearance), plasma AA, and glucagon levels, as well as 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 · 1.73 m-2); 2) low-AA solution (150 mg · min-1 · 1.73 m-2); 3) low AA + 2,000 ml/1.73 m2 of 0.23{\%} saline solution; 4) high AA + 0.23{\%} saline; 5) high AA + 0.45{\%} saline; and 6) 0.45{\%} saline alone. The glomerular filtration rate (GFR) rise induced by the high-AA solution was similar to that induced by the low-AA solution (ΔGFR = +24 ± 6 and +20.2 ± 7 ml · min-1 · 1.73 m-2, 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 (ΔGFR = +6.6 ± 10.1 and +11.4 ± 8.3 ml · min-1 · 1.73 m-2, 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 he blunted by hypotonic saline infusion, possibly through an acute modification of renal sodium handling and extracellular volume.",
keywords = "Glucagon, Renal hemodynamics, Sodium handling, Urea excretion",
author = "Aldo Claris-Appiani and Tirelli, {Amedea S.} and Gianluigi Ardissino and Valeria Dacc{\`o} and Eugenia Moretto and Carlo Corbetta and Laura Guidi and Assael, {Baroukh M.}",
year = "1999",
month = "1",
language = "English",
volume = "276",
journal = "American Journal of Physiology",
issn = "0363-6119",
publisher = "American Physiological Society",
number = "1 45-1",

}

TY - JOUR

T1 - Hypotonic saline infusion alters the renal response to amino acids in men

AU - Claris-Appiani, Aldo

AU - Tirelli, Amedea S.

AU - Ardissino, Gianluigi

AU - Daccò, Valeria

AU - Moretto, Eugenia

AU - Corbetta, Carlo

AU - Guidi, Laura

AU - Assael, Baroukh M.

PY - 1999/1

Y1 - 1999/1

N2 - 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, p-aminohippurate clearance), plasma AA, and glucagon levels, as well as 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 · 1.73 m-2); 2) low-AA solution (150 mg · min-1 · 1.73 m-2); 3) low AA + 2,000 ml/1.73 m2 of 0.23% saline solution; 4) high AA + 0.23% saline; 5) high AA + 0.45% saline; and 6) 0.45% saline alone. The glomerular filtration rate (GFR) rise induced by the high-AA solution was similar to that induced by the low-AA solution (ΔGFR = +24 ± 6 and +20.2 ± 7 ml · min-1 · 1.73 m-2, 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 (ΔGFR = +6.6 ± 10.1 and +11.4 ± 8.3 ml · min-1 · 1.73 m-2, 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 he blunted by hypotonic saline infusion, possibly through an acute modification of renal sodium handling and extracellular volume.

AB - 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, p-aminohippurate clearance), plasma AA, and glucagon levels, as well as 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 · 1.73 m-2); 2) low-AA solution (150 mg · min-1 · 1.73 m-2); 3) low AA + 2,000 ml/1.73 m2 of 0.23% saline solution; 4) high AA + 0.23% saline; 5) high AA + 0.45% saline; and 6) 0.45% saline alone. The glomerular filtration rate (GFR) rise induced by the high-AA solution was similar to that induced by the low-AA solution (ΔGFR = +24 ± 6 and +20.2 ± 7 ml · min-1 · 1.73 m-2, 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 (ΔGFR = +6.6 ± 10.1 and +11.4 ± 8.3 ml · min-1 · 1.73 m-2, 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 he blunted by hypotonic saline infusion, possibly through an acute modification of renal sodium handling and extracellular volume.

KW - Glucagon

KW - Renal hemodynamics

KW - Sodium handling

KW - Urea excretion

UR - http://www.scopus.com/inward/record.url?scp=0032950474&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0032950474&partnerID=8YFLogxK

M3 - Article

C2 - 9887089

AN - SCOPUS:0032950474

VL - 276

JO - American Journal of Physiology

JF - American Journal of Physiology

SN - 0363-6119

IS - 1 45-1

ER -