Dietary protein suppresses feedback control of glomerular filtration in rats.

Seney, Frank D.; Wright, Fay

doi:10.1172/jci111732

Cited by 76 publications

(33 citation statements)

References 33 publications

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“…The mechanisms that mediate the acute renal response to a protein or amino acid load are not well defined, although some authors have considered that this response in induced by glucagon (Parving et al 1985), a liver-derived renal vasodilator (Premen 1985;Dratwa et al 1984) glomerulopressin (Alvestrand and Bergstrom 1984), tobule-glomerular feedback (Seney and Wright 1985), prostaglandins (Krishna et al 1988). In the present study, the mechanism of this response was not elucidated, but the finding that loading a vegetable protein did not increase GFR might provide some clarification.…”

Section: Discussionmentioning

confidence: 99%

Effects of acute protein loads of different sources on renal function of patients with diabetic nephropathy.

Nakamura

Takasawa

Kashara

et al. 1989

Tohoku J. Exp. Med.

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To evaluate effects of acute loading of different proteins on renal function, glomerular filtration rate (GFR), albumin excretion rate (AER), and concentrations of plasma amino acids, 11 normal volunteers and 20 diabetic patients were studied before and after eating 1.0 g/kg body weight of either tuna fish meal or bean curd on separate days. In normal subjects, the mean baseline GFR was 115.8+9.5 ml/min/1.73 m2, and the mean GFRs after ingestion of tuna fish meal were 134.1± 15.5 (1 hr), 146.2 + 18.8 (2 hr), and 157.8±21.2 (3 hr), respectively. GFR did not significantly increase in normal subjects after ingestion of bean curd. GFR in diabetic patients with normoalbuminuria after ingestion of each protein was similar to the response in normal subjects. In diabetic patients with microalbuminuria, GFR did not significantly increase after ingestion of each protein. In diabetes with macroalbuminuria, GFR decreased after ingestion of tuna fish meal and did not significantly change after intake of bean curd. In both normal subjects and diabetic patients, urinary AER did not increase after each kind of protein loading. Plasma concentrations of alanine, glycine, and arginine, known to induce glomerular hyperfiltration, increased to a greater degree after ingestion of tuna fish meal than after administration of bean curd. These findings suggest that responses of GFR to acute protein loading may differ according to the amino acid composition of the protein ingested and to the stage of diabetic nephropathy. Diabetic nephropathy ; GFR ; glomerular hyperfiltration ; proteins of different sources ; composition of amino acids An elevated glomerular filtration rate (GFR) in uncomplicated type 1 (insulin dependent) diabetic patients has been confirmed for many years. As to the clinical significance of this phenomenon, Mogensen (1971Mogensen ( , 1976 recently reported that glomerular hyperfiltration in type 1 diabetes with an early stage of diabetic nephropathy might play an important role in subsequent development of late diabetic nephropathy.Although the exact mechanism that induces glomerular

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Section: Discussionmentioning

confidence: 99%

Effects of acute protein loads of different sources on renal function of patients with diabetic nephropathy.

Nakamura

Takasawa

Kashara

et al. 1989

Tohoku J. Exp. Med.

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“…Examples include the hyperfiltration observed with protein feeding (90) and uninephrectomy (19,24) and in pregnancy (11). Evidence implicates a chronic resetting of TGF in such settings and in the hyperfiltration seen in diabetes (141,158). Longer-acting adaptations to elevated pressure may also exist, and such mechanisms could contribute to the observed lack of impact of acute autoregulatory impairment on volume homeostasis.…”

Section: Regulation Of Rbf and Gfr Independent Of Autoregulatory Respmentioning

confidence: 99%

Renal autoregulation: new perspectives regarding the protective and regulatory roles of the underlying mechanisms

Loutzenhiser

Griffin²,

Bidani³

2006

American Journal of Physiology-Regulatory, Integrative and Comp

237

244

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dani. Renal autoregulation: new perspectives regarding the protective and regulatory roles of the underlying mechanisms. Am J Physiol Regul Integr Comp Physiol 290: R1153-R1167, 2006. doi:10.1152/ajpregu.00402.2005.-When the kidney is subjected to acute increases in blood pressure (BP), renal blood flow (RBF) and glomerular filtration rate (GFR) are observed to remain relatively constant. Two mechanisms, tubuloglomerular feedback (TGF) and the myogenic response, are thought to act in concert to achieve a precise moment-by-moment regulation of GFR and distal salt delivery. The current view is that this mechanism insulates renal excretory function from fluctuations in BP. Indeed, the concept that renal autoregulation is necessary for normal renal function and volume homeostasis has long been a cornerstone of renal physiology. This article presents a very different view, at least regarding the myogenic component of this response. We suggest that its primary purpose is to protect the kidney against the damaging effects of hypertension. The arguments advanced take into consideration the unique properties of the afferent arteriolar myogenic response that allow it to protect against the oscillating systolic pressure and the accruing evidence that when this response is impaired, the primary consequence is not a disturbed volume homeostasis but rather an increased susceptibility to hypertensive injury. It is suggested that redundant and compensatory mechanisms achieve volume regulation, despite considerable fluctuations in distal delivery, and the assumed moment-by-moment regulation of renal hemodynamics is questioned. Evidence is presented suggesting that additional mechanisms exist to maintain ambient levels of RBF and GFR within normal range, despite chronic alterations in BP and severely impaired acute responses to pressure. Finally, the implications of this new perspective on the divergent roles of the myogenic response to pressure vs. the TGF response to changes in distal delivery are considered, and it is proposed that in addition to TGF-induced vasoconstriction, vasodepressor responses to reduced distal delivery may play a critical role in modulating afferent arteriolar reactivity to integrate the regulatory and protective functions of the renal microvasculature. renal microcirculation; afferent arteriole; myogenic; tubuloglomerular feedback ONE OF THE MOST STRIKING CHARACTERISTICS of the renal circulation is the ability of the kidney to maintain a constant renal blood flow (RBF) and glomerular filtration rate (GFR) as renal perfusion pressure is altered. The dual regulation of both RBF and GFR is achieved by proportionate changes in the preglomerular resistance and is believed to be mediated by two mechanisms, tubuloglomerular feedback (TGF) and the renal myogenic response. TGF involves a flow-dependent signal that is sensed at the macula densa and alters tone in the adjacent segment of the afferent arteriole via a mechanism that remains controversial but likely involves adenosine and/or ATP (30,80,144). The myo...

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“…Microperfusion studies by Seney et al (68) determined that protein-induced increases in GFR result from changes in the tubuloglomerular feedback (TGF) system. Their studies found that the sensing mechanism of the TGF system was rendered less responsive by high protein intake and that the diminished TGF was caused, at least in part, by a reduced early distal NaCl concentration, without a change in early distal tubule osmolality (69). However, the cause of the reduced luminal NaCl concentration remains unknown.…”

Section: Urea Recycling and Regulation Of Gfr By High-protein Dietsmentioning

confidence: 99%

Urea and Renal Function in the 21st Century

Fenton¹,

Knepper²

2007

Journal of the American Society of Nephrology

115

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Since the turn of the 21st century, gene knockout mice have been created for all major urea transporters that are expressed in the kidney: the collecting duct urea transporters UT-A1 and UT-A3, the descending thin limb isoform UT-A2, and the descending vasa recta isoform UT-B. This article discusses the new insights that the results from studies in these mice have produced in the understanding of the role of urea in the urinary concentrating mechanism and kidney function. Following is a summary of the major findings: (1) Urea accumulation in the inner medullary interstitium depends on rapid transport of urea from the inner medullary collecting duct (IMCD) lumen via UT-A1 and/or UT-A3; (2) as proposed by Robert Berliner and colleagues in the 1950s, the role of IMCD urea transporters in water conservation is to prevent a urea-induced osmotic diuresis; (3) the absence of IMCD urea transport does not prevent the concentration of NaCl in the inner medulla, contrary to what would be predicted from the passive countercurrent multiplier mechanism in the form proposed by Kokko and Rector and Stephenson; (4) deletion of UT-B (vasa recta isoform) has a much greater effect on urinary concentration than deletion of UT-A2 (descending limb isoform), suggesting that the recycling of urea between the vasa recta and the renal tubules quantitatively is less important than classic countercurrent exchange; and (5) urea reabsorption from the IMCD and the process of urea recycling are not important elements of the mechanism of protein-induced increases in GFR. In addition, the clinical relevance of these studies is discussed, and it is suggested that inhibitors that specifically target collecting duct urea transporters have the potential for clinical use as potassium-sparing diuretics that function by creation of urea-dependent osmotic diuresis.

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Dietary protein suppresses feedback control of glomerular filtration in rats.

Cited by 76 publications

References 33 publications

Effects of acute protein loads of different sources on renal function of patients with diabetic nephropathy.

Effects of acute protein loads of different sources on renal function of patients with diabetic nephropathy.

Renal autoregulation: new perspectives regarding the protective and regulatory roles of the underlying mechanisms

Urea and Renal Function in the 21st Century

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