Effect of specific amino acid groups on renal hemodynamics in humans

Castellino, Pietro; Levin, Robert D.; Shohat, J; DeFronzo, Ralph A.

doi:10.1152/ajprenal.1990.258.4.f992

Cited by 25 publications

(23 citation statements)

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“…We detected no change in the urea excretion rate, urea filtered load or plasma glucagon/insulin ratio and, furthermore, the observed decrease in plasma ornithine levels (and corresponding increase in plasma arginine levels) induced by the EAA infusion could be interpreted as indicating reduced ureagenesis. Our data are in line with the demonstration that GFR does not increase after administration of D-serine and cystine [2] or branched-chain AA [3][4][5] which are all AA that are not metabolized in the splanchnic region, whereas GFR is stimulated by a mixture of gluconeogenetic AAs [3].…”

Section: Discussionsupporting

confidence: 91%

“…A number of clues indicate that this intermediate step may occur in the splanchnic region. Branchedchain AA, which are poorly metabolized at the splanchnic level stimulate renal hemodynamics less than those which are rapidly transaminated and deaminated in the liver (serine, proline, alanine, dicarboxylic acids and the gluconeogenetic AA in general) [2,[3][4][5]. Moreover, glucagon has been repeatedly proposed as an important element in AA-induced renal hyperfiltration [3,[6][7][8][9].…”

Section: Introductionmentioning

confidence: 99%

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Metabolic Factors in the Renal Response to Amino Acid Infusion

et al. 1998

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In order to investigate the renal effects of amino acids (AA) with different metabolic fate, we compared the changes in glomerular and tubular function, nitrogen metabolism and glucoregulatory hormones in 7 volunteers during two infusions, one of a complete solution of amino acids (MIX-AA), which included five AA electively metabolized at the splanchnic level, and the other of a solution containing only essential AA (EAA), which escape splanchnic metabolism. MIX-AA increased GFR and RPF (from 104 ± 6 to 122 ± 13 and from 488 ± 46 to 572 ± 34 ml/min/1.73 m²), stimulated splanchnic metabolism as demonstrated by rises in urinary urea excretion (from 20.7 ± 2 to 30.6 ± 7.5 mg/min/1.73 m²) and the plasma glucagon/insulin ratio (from 21.4 ± 13 to 26.7 ± 15), and caused increases in fractional excretion of AA, FeNa and free-water clearance. During MIX-AA infusion significant correlations were observed between the individual values of GFR and the urea excretion rate (r = 0.66), and between GFR modifications (ΔGFR) and the plasma glucagon/plasma insulin ratio (r = 0.40). No change in renal function, urea excretion and the glucagon/insulin ratio was observed with EAA. An intermediate splanchnic step (increased plasma glucagon/insulin ratio and ureagenesis) seems necessary in the pathway leading to the nonessential AA-induced rise in GFR; this might stimulate an ultimate intrarenal pathway (possibly involving the diluting segment) via a still undefined mechanism.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Metabolic Factors in the Renal Response to Amino Acid Infusion

et al. 1998

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“…This observation is in agreement with the study of Premen and Dobbins, 22 who have shown that amino acid combinations of L-but not r>isomers elevated RPF and GFR, and with Castellino et al, 23 who demonstrated that RPF and GFR were increased by a solution of gluconeogenic amino acids containing L-arginine. NO may have taken part in the renal hemodynamic response to amino acids in our patients during a normal salt diet.…”

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confidence: 92%

Renal response to amino acid infusion in essential hypertension.

et al. 1994

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In the present study, we evaluated the renal response to a 4-hour infusion of amino acids in essential hypertensive patients, as well as the effects that dietary sodium restriction and enalapril (a converting enzyme inhibitor) had on this renal response. During normal sodium intake, amino acid infusion significantly increased renal plasma flow from 383±58 to 478±51 mL/min and glomerular filtration rate from 82±8 to 100±13 mL/min. All these effects were abolished when the patients received a low sodium diet (40 mmol/d) for 3 days before the amino acid infusion. The administration of enalapril to the patients during sodium restriction restored the amino acid-induced increment in renal plasma flow (from 388±35 to 537±48 mL/min) and glomerular filtration rate (from 88±9 to 103±10 mL/min). Mean arterial pressure remained unaltered under all experimental conditions. The results show that in patients with essential hypertension dietary sodium restriction prevents amino acid-induced increments in glomerular filtration rate and renal plasma flow and that this effect is restored during the simultaneous administration of enalapril. 2 that a high protein intake produces a significant increase in both renal plasma flow (RPF) and glomerular filtration rate (GFR). These effects have been held responsible for accelerating glomerular damage, mainly in patients with preexisting renal insufficiency.3 However, it is not known if similar deleterious effects are exerted by high-protein diets in patients with essential hypertension. Intravenous administration of an amino acid combination used in parenteral nutrition therapy increases RPF and GFR 4 in normotensive volunteers. In these normotensive individuals, dietary sodium restriction inhibits the renal responses to amino acid infusion; however, administration of a converting enzyme inhibitor during sodium restriction restores the vasodilator renal response. 4 A similar renal response should not be assumed for patients with essential hypertension. In these patients the kidney endures higher sympathetic tone 5 and higher renal vascular reactivity. 6 Likewise, angiotensin II (Ang II) may contribute to the renal vasoconstriction of hypertension.7 Hence, renal vasoconstriction is a frequent if not constant finding in essential hypertension. We speculated that these pressor stimuli, seen in hypertensive but not in normotensive individuals, could restrict a protein-induced renal vasodilation. Furthermore, we felt the basis for such a notion could lie in the activity of the renin-angiotensin system. This study was designed to answer the following questions: (1) Is the kidney of patients with essential hypertension able to increase RPF and GFR in response to an From Institute) Privado de Especialidades Medicas and National University of Cordoba, Argentina (LJ., J.C.C., E.P.-A.), and the Department of Physiology, Division of Hypertension, Mayo Clinic, Rochester, Minn (J.C.R.).This manuscript from the Mayo dink: was sent to Gerald F. DiBona, Editor-in-Chief, for review by expert refere...

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“…In contrast, glucagon infusion increasing plasma concentration to 900 pg/ ml or above (5) (a concentration usually achieved in the portal circulation) or infusion of lower amounts in the portal vein (10) does increase GFR. It has been proposed that the rise in GFR could depend on the liberation by the liver of a mediator or metabolite derived from amino acid metabolism (6,15,16,21). A putative liver-derived vasoactive mediator glomerulopressin has not been well characterized to date (for review see reference 20).…”

Section: Groups Plasma Urea (Mm)mentioning

confidence: 99%

“…It has been proposed that glucagon could induce the release from the liver of a vasoactive hormone, glomerulopressin, influencing the resistance of renal arterioles (17,18, and for reviews see references 19 and 20). Other studies have suggested that the link between the liver and the kidney could be a compound(s) derived from the metabolism of amino acids by the liver (21)(22)(23). The nature of this compound has not yet been determined.…”

Section: Introductionmentioning

confidence: 99%

Cyclic AMP is a hepatorenal link influencing natriuresis and contributing to glucagon-induced hyperfiltration in rats.

Ahloulay¹,

Déchaux²,

Hassler³

et al. 1996

J. Clin. Invest.

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The effects of glucagon (G) on proximal tubule reabsorption (PTR) and GFR seem to depend on a prior action of this hormone on the liver resulting in the liberation of a mediator and/or of a compound derived from amino acid metabolism. This study investigates in anesthetized rats the possible contribution of cAMP and urea, alone and in combination with a low dose of G, on phosphate excretion (known to depend mostly on PTR) and GFR. After a 60-min control period, cAMP (5 nmol/min ϫ 100 grams of body weight [BW]) or urea (2.5 mol/min ϫ 100 grams BW) was infused intravenously for 200 min with or without G (1.2 ng/min ϫ 100 grams BW, a physiological dose which, alone, does not influence PTR or GFR). cAMP increased markedly the excretion of phosphate and sodium ( ϩ 303 and ϩ 221%, respectively, P Ͻ 0.01 for each) but did not alter GFR. Coinfusion of cAMP and G induced the same tubular effects but also induced a 20% rise in GFR ( P Ͻ 0.05). Infusion of urea, with or without G, did not induce significant effects on PTR or GFR. After G infusion at increasing doses, the increase in fractional excretion of phosphate was correlated with a simultaneous rise in plasma cAMP concentration and reached a maximum for doubling of plasma cAMP. These results suggest that cAMP, normally released by the liver into the blood under the action of G, ( a ) is probably an essential hepatorenal link regulating the intensity of PTR, and ( b ) contributes, in conjunction with specific effects of G on the nephron, to the regulation of GFR. ( J. Clin. Invest. 1996. 98: 2251-2258.)

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Effect of specific amino acid groups on renal hemodynamics in humans

Cited by 25 publications

References 0 publications

Metabolic Factors in the Renal Response to Amino Acid Infusion

Metabolic Factors in the Renal Response to Amino Acid Infusion

Renal response to amino acid infusion in essential hypertension.

Cyclic AMP is a hepatorenal link influencing natriuresis and contributing to glucagon-induced hyperfiltration in rats.

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