title: Renal functional reserve in pigs: renal haemodynamics, renal tubular function and salt and water homeostatic hormones during amino acid and dopamine stimulation.
abstract: The purpose of the study was to evaluate renal functional reserve [RFR is the difference between glomerular filtration rate (GFR) at rest and maximal GFR after stimulation] in a controlled study in normal pigs. Our basic hypothesis was that a decreased RFR may be used as an early indicator of renal deterioration, i.e. a test to disclose significant obstruction as opposed to simple dilatation in hydronephrosis. During various forms of stimulation (amino acids, captopril and dopamine), we measured changes in GFR, renal plasma flow (RPF), tubular reabsorption of sodium and water, net uptake from plasma to the kidney of three salt and water homeostatic hormones (angiotensin II, aldosterone and atrial natriuretic peptide) and of glucagon, which is thought to play a key role as mediator of the GFR increase during amino acid infusion. We found the largest GFR increase during combined infusion of amino acids and dopamine (+13%), but compared with a non-stimulated control group, the GFR increase was statistically non-significant. RPF increased by 57% during stimulation with amino acids plus dopamine (P < 0.001), while tubular reabsorption of sodium and water, and renal uptake of angiotensin II, aldosterone and atrial natriuretic peptide showed no significant differences between control and stimulation groups. The renal uptake of glucagon increased significantly during amino acid stimulation with no concomitant GFR increase. We conclude that in this experimental, non-obstructed model, RFR is a very insensitive measure, which cannot be used to discriminate between obstruction and simple dilatation in hydronephrosis. Further, our study does not support the hypothesis that glucagon is involved in GFR changes after amino acids.
authors.affiliation: Institute of Experimental Clinical Research, University of Aarhus, Denmark.
authors.forename: E U
authors.initials: EU
authors.lastname: Poulsen
authors.forename: J
authors.initials: J
authors.lastname: Frøkiaer
authors.forename: T M
authors.initials: TM
authors.lastname: Jørgensen
authors.forename: E B
authors.initials: EB
authors.lastname: Pedersen
authors.forename: M
authors.initials: M
authors.lastname: Rehling
mesh_terms: D000450:Aldosterone / Q000097:blood; D000596:Amino Acids / Q000494:pharmacology*; D000804:Angiotensin II / Q000097:blood; D000818:Animals; D009320:Atrial Natriuretic Factor / Q000097:blood; D001794:Blood Pressure; D002216:Captopril / Q000494:pharmacology*; D004298:Dopamine / Q000494:pharmacology*; D005260:Female; D005919:Glomerular Filtration Rate; D005934:Glucagon / Q000493:pharmacokinetics; D006400:Hematocrit; D006439:Hemodynamics / Q000187:drug effects; D007668:Kidney / Q000254:growth & development / Q000378:metabolism / Q000502:physiology*; D007684:Kidney Tubules / Q000502:physiology*; D009399:Nephrons / Q000502:physiology; D009929:Organ Size; D011674:Pulse; D012079:Renal Circulation / Q000502:physiology; D012964:Sodium / Q000097:blood / Q000652:urine; D013552:Swine / Q000502:physiology*; D014655:Vascular Resistance
chemical_list: D000596:Amino Acids; D000804:Angiotensin II; D000450:Aldosterone; D009320:Atrial Natriuretic Factor; D005934:Glucagon; D002216:Captopril; D012964:Sodium; D004298:Dopamine