OBJECTIVES: Previous studies demonstrated that protein meals and amino acid (AA) infusions increase glomerular filtration rate (GFR) and renal plasma flow (RPF) and that somatostatin (SRIH) infusion inhibits these increments. We tested whether a single AA such as alanine could increase GFR and RPF and whether the changes in GFR and RPF could be explained on the basis of changes in glucagon, growth hormone (GH), and insulin. RESEARCH DESIGN AND METHODS: In the first experiment, alanine was infused with or without SRIH in five normal subjects. In the second experiment, five other subjects were infused with SRIH on three separate occasions. In a control study, insulin, glucagon, and GH were given at replacement doses; in a hyperglucagonemia study, glucagon was given at a rate of 0.2 microgram.kg-1.h-1 (hypoglucagonemia); and in a high GH study, GH was given at a rate of 2 micrograms.kg-1.h-1. GFR and RPF were measured using insulin and para-aminohippurate, respectively. RESULTS: Alanine increased GFR and RPF, whereas SRIH inhibited these changes (P < 0.05). Hyperglucagonemia or high GH with or without insulin failed to increase RPF or GFR. CONCLUSIONS: A single AA such as alanine increases GFR and RPF, and this increase is dependent on a factor inhibited by SRIH. Although GH, glucagon, and insulin are factors inhibited by SRIH, none of these factors explains the changes in RPF and GFR in our acute studies.
OBJECTIVES: Previous studies demonstrated that protein meals and amino acid (AA) infusions increase glomerular filtration rate (GFR) and renal plasma flow (RPF) and that somatostatin (SRIH) infusion inhibits these increments. We tested whether a single AA such as alanine could increase GFR and RPF and whether the changes in GFR and RPF could be explained on the basis of changes in glucagon, growth hormone (GH), and insulin. RESEARCH DESIGN AND METHODS: In the first experiment, alanine was infused with or without SRIH in five normal subjects. In the second experiment, five other subjects were infused with SRIH on three separate occasions. In a control study, insulin, glucagon, and GH were given at replacement doses; in a hyperglucagonemia study, glucagon was given at a rate of 0.2 microgram.kg-1.h-1 (hypoglucagonemia); and in a high GH study, GH was given at a rate of 2 micrograms.kg-1.h-1. GFR and RPF were measured using insulin and para-aminohippurate, respectively. RESULTS:Alanine increased GFR and RPF, whereas SRIH inhibited these changes (P < 0.05). Hyperglucagonemia or high GH with or without insulin failed to increase RPF or GFR. CONCLUSIONS: A single AA such as alanine increases GFR and RPF, and this increase is dependent on a factor inhibited by SRIH. Although GH, glucagon, and insulin are factors inhibited by SRIH, none of these factors explains the changes in RPF and GFR in our acute studies.
Authors: Bruce A Perkins; Robert G Nelson; Betsy E P Ostrander; Kristina L Blouch; Andrzej S Krolewski; Bryan D Myers; James H Warram Journal: J Am Soc Nephrol Date: 2005-03-23 Impact factor: 10.121
Authors: Stephane Walrand; Kevin R Short; Maureen L Bigelow; Andrew J Sweatt; Susan M Hutson; K Sreekumaran Nair Journal: Am J Physiol Endocrinol Metab Date: 2008-08-12 Impact factor: 4.310