Tubuloglomerular feedback and glomerular morphology in Goldblatt hypertensive rats on varying protein diets

Schnermann, Jürgen; Gokel, M; Weber, Peter; Schubert, G; Briggs, Josephine P.

doi:10.1038/ki.1986.30

Cited by 22 publications

(13 citation statements)

References 32 publications

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“…The role of hypertension in this lesion is further demonstrated by the fact that lowering BP results in proportionate reductions in injury (20,59). Similar relationships between impaired renal autoregulation and increased renal susceptibility to hypertensive injury have been noted in the DOCA/salt model of hypertension (72,109), and in the nonclipped kidney of the 2K/1C model (124,133). Moreover, interventions that alter autoregulatory capacity, such as dietary protein restriction or calcium channel blockers, produce corresponding changes in susceptibility to hypertensive injury in models of CKD (57,60,62) and in the DOCA/ salt and 2K/1C models of hypertension (92,133).…”

Section: Consequences Of Impaired Renal Autoregulation On Renal Protementioning

confidence: 61%

“…The difficulties involve the same problems impeding attempts to assess the individual contributions of these two interacting systems when autoregulation is intact. In the DOCA/salt, 2K/1C, and the 5/6 ablation models, TGF responses of the affected kidney are reported to be blunted or reset (109,124,128,133), but a concurrent defect in myogenic reactivity is not excluded (e.g., Ref. 70).…”

Section: Consequences Of Impaired Renal Autoregulation On Renal Protementioning

confidence: 99%

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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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Section: Consequences Of Impaired Renal Autoregulation On Renal Protementioning

confidence: 61%

Section: Consequences Of Impaired Renal Autoregulation On Renal Protementioning

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

View full text Add to dashboard Cite

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“…Such data point to changes in the func tion of the TG feedback mechanism [1,2] due to a modification of the signal eliciting the TG feedback response [3]. However, one should take advantage of the present knowledge re garding the activity of the Na+-H + exchanger following an acute rise in GFR.…”

Section: Discussionmentioning

confidence: 99%

Tubular Function by Lithium Clearance, Plasma Amino Acids and Hormones following a Meat Meal in Childhood

Santo¹,

Coppola²,

Coscarella³

et al. 1991

Kidney Blood Press Res

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Tubular function was measured by lithium clearance (C_Li) and by its derived formulae before and after the transient increase (lasting 90min) in glomerular filtration rate (GFR) following a meat meal (2g protein/kg body weight) in 12 normal children. Three baseline and 4 clearances after the meal were obtained, each lasting 30min. The mean baseline C_Li was 23.1 ± 1.64ml/min/1.73m². At peak GFR response (60min from starting the meal), C_Li averaged 27.6 ± 2.4ml/min/1.73m² (p < 0.025vs. baseline) and it was further increased (32.2 ± 5.04ml/ min/1.73m², p < 0.01 vs. baseline) 120min after starting the meal, while GFR returned to baseline values. Fractional lithium excretion averaged 0.23 ± 0.04 at baseline and increased continuously after the meat meal and, at completion of the study, it averaged 0.38 ± 0.07 (p < 0.025vs. baseline). The distal absolute and fractional sodium reabsorption increased throughout the studies following the meal and peaked at 120 min. The functional changes were associated with a statistically significant increase in the plasma concentration of insulin, glucagon, and total amino acids after the meal. The latter at the end of the study was almost doubled (5,600 ± 780 versus 3,200 µM at baseline, p < 0.01). The data indicate that the tubulo glomerular feedback mechanism operates normally after a meat meal. The finding on increased distal sodium reabsorption might point to the existence of an insulin-dependent mechanism.

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“…Renal autoregulation is impaired in the RRM, DOCA/salt, and DS rat models of hypertension and in salt-supplemented SHRSP (109,169,194,230,247,252). The glomerular capillary hydraulic pressure (P GC ) and the blood flow in cortical glomeruli of SHR are maintained during elevation of the renal perfusion pressure by highly effective autoregulation (121,233,317).…”

Section: Renal Autoregulationmentioning

confidence: 99%

Oxidative Stress in Hypertension: Role of the Kidney

Araújo

Wilcox

2014

Antioxidants & Redox Signaling

160

131

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Significance: Renal oxidative stress can be a cause, a consequence, or more often a potentiating factor for hypertension. Increased reactive oxygen species (ROS) in the kidney have been reported in multiple models of hypertension and related to renal vasoconstriction and alterations of renal function. Nicotinamide adenine dinucleotide phosphate oxidase is the central source of ROS in the hypertensive kidney, but a defective antioxidant system also can contribute. Recent Advances: Superoxide has been identified as the principal ROS implicated for vascular and tubular dysfunction, but hydrogen peroxide (H 2 O 2 ) has been implicated in diminishing preglomerular vascular reactivity, and promoting medullary blood flow and pressure natriuresis in hypertensive animals. Critical Issues and Future Directions: Increased renal ROS have been implicated in renal vasoconstriction, renin release, activation of renal afferent nerves, augmented contraction, and myogenic responses of afferent arterioles, enhanced tubuloglomerular feedback, dysfunction of glomerular cells, and proteinuria. Inhibition of ROS with antioxidants, superoxide dismutase mimetics, or blockers of the reninangiotensin-aldosterone system or genetic deletion of one of the components of the signaling cascade often attenuates or delays the onset of hypertension and preserves the renal structure and function. Novel approaches are required to dampen the renal oxidative stress pathways to reduced O 2 -rather than H 2 O 2 selectivity and/or to enhance the endogenous antioxidant pathways to susceptible subjects to prevent the development and renaldamaging effects of hypertension. Antioxid. Redox Signal. 20, 74-101.

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Tubuloglomerular feedback and glomerular morphology in Goldblatt hypertensive rats on varying protein diets

Cited by 22 publications

References 32 publications

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

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

Tubular Function by Lithium Clearance, Plasma Amino Acids and Hormones following a Meat Meal in Childhood

Oxidative Stress in Hypertension: Role of the Kidney

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