Autoregulation and tubuloglomerular feedback in juxtamedullary glomerular arterioles

Casellas, Daniel; Moore, Leon C.

doi:10.1152/ajprenal.1990.258.3.f660

Cited by 93 publications

(99 citation statements)

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“…Just and Arendshorst (85) reported a delay in pressure-induced vasodilation of 530 ms, considerably shorter than the 1-s delay we found in the hydronephrotic kidney (97), but nevertheless significantly longer than the delay in vasoconstriction in the intact kidney. Longer delays in the offset vs. onset of vasoconstrictor responses induced by changes in loop of Henle flow are also reported (29,37). The dilation observed at the afferent arteriolar level was best fit to a biexponential function, but achieved 66% of the maximal response within ϳ3 s (97), similar to overall rate constant reported by Just and Arendshorst (2.6 s; Ref.…”

Section: Renal Myogenic Response To the Oscillating Systolic Pressuresupporting

confidence: 65%

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: Renal Myogenic Response To the Oscillating Systolic Pressuresupporting

confidence: 65%

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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“…These experiments used the in vitro juxtamedullary (JM) nephron preparation (26,27) to characterize the renal vascular actions of exogenous anadamide. In brief, male Sprague-Dawley rats (200-250 g) were anesthetized with 110 mg/kg Inactin (Research Biochemicals, Inc., Natick, MA).…”

Section: Methodsmentioning

confidence: 99%

“…In this study, all drugs were applied abluminally via the superfusate. The responses of JM midafferent arteriole (mAA) segments were quantified as the change in lumen diameter via videomicroscopy as previously described (27). Results were subjected to one-or two-way ANOVA on repeated measures and Student-Newman-Kuels or Dunnett's multiple comparison tests using SigmaStat software (Jandel Scientific, San Raphael, CA).…”

Section: Methodsmentioning

confidence: 99%

Production and physiological actions of anandamide in the vasculature of the rat kidney.

Deutsch¹,

Goligorsky²,

Schmid³

et al. 1997

J. Clin. Invest.

327

276

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The endogenous cannabinoid receptor agonist anandamide is present in central and peripheral tissues. As the kidney contains both the amidase that degrades anandamide and transcripts for anandamide receptors, we characterized the molecular components of the anandamide signaling system and the vascular effects of exogenous anandamide in the kidney. We show that anandamide is present in kidney homogenates, cultured renal endothelial cells (

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“…As discussed in more detail by Inscho, the kidney is a highly efficient autoregulatory organ and it is generally accepted that the TGF mechanism is responsible, at least in part, for this behaviour [90][91][92][93]. Thus, in response to an increase in blood pressure, there would be a transient elevation in GFR, leading to increased tubular flow into the proximal tubule.…”

Section: Atp As a Mediator Of Tgfmentioning

confidence: 99%

ATP as a mediator of macula densa cell signalling

Bell

Komlósi

Zhang

2009

Purinergic Signalling

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Within each nephro-vascular unit, the tubule returns to the vicinity of its own glomerulus. At this site, there are specialised tubular cells, the macula densa cells, which sense changes in tubular fluid composition and transmit information to the glomerular arterioles resulting in alterations in glomerular filtration rate and blood flow. Work over the last few years has characterised the mechanisms that lead to the detection of changes in luminal sodium chloride and osmolality by the macula densa cells. These cells are true "sensor cells" since intracellular ion concentrations and membrane potential reflect the level of luminal sodium chloride concentration. An unresolved question has been the nature of the signalling molecule(s) released by the macula densa cells. Currently, there is evidence that macula densa cells produce nitric oxide via neuronal nitric oxide synthase (nNOS) and prostaglandin E 2 (PGE 2 ) through cyclooxygenase 2 (COX 2)-microsomal prostaglandin E synthase (mPGES). However, both of these signalling molecules play a role in modulating or regulating the macula-tubuloglomerular feedback system. Direct macula densa signalling appears to involve the release of ATP across the basolateral membrane through a maxi-anion channel in response to an increase in luminal sodium chloride concentration. ATP that is released by macula densa cells may directly activate P2 receptors on adjacent mesangial cells and afferent arteriolar smooth muscle cells, or the ATP may be converted to adenosine. However, the critical step in signalling would appear to be the regulated release of ATP across the basolateral membrane of macula densa cells.

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Autoregulation and tubuloglomerular feedback in juxtamedullary glomerular arterioles

Cited by 93 publications

References 0 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

Production and physiological actions of anandamide in the vasculature of the rat kidney.

ATP as a mediator of macula densa cell signalling

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