ATP as a mediator of macula densa cell signalling

Bell, P. Darwin; Komlósi, Péter; Zhang, Zhiren

doi:10.1007/s11302-009-9148-0

Cited by 57 publications

(45 citation statements)

References 108 publications

(96 reference statements)

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“…The role of molecular densa in providing TGF to afferent vessels and signaling pathways leading to changes in renovascular constriction and glomerular filtration rate has been better elucidated recently (Ren et al, 2004;Bell et al, 2009). Cl entry to the molecular densa cells has been shown to cause depolarization to the basal lateral membrane via Cl channels (Bell et al, 1989).…”

Section: Pathological Effects Of Saline On Renal Hemodynamicsmentioning

confidence: 99%

0.9% saline is neither normal nor physiological

Sun

Yap

et al. 2016

J. Zhejiang Univ. Sci. B

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Abstract:The purpose of this review is to objectively evaluate the biochemical and pathophysiological properties of 0.9% saline (henceforth: saline) and to discuss the impact of saline infusion, specifically on systemic acid-base balance and renal hemodynamics. Studies have shown that electrolyte balance, including effects of saline infusion on serum electrolytes, is often poorly understood among practicing physicians and inappropriate saline prescribing can cause increased morbidity and mortality. Large-volume (>2 L) saline infusion in healthy adults induces hyperchloremia which is associated with metabolic acidosis, hyperkalemia, and negative protein balance. Saline overload (80 ml/kg) in rodents can cause intestinal edema and contractile dysfunction associated with activation of sodium-proton exchanger (NHE) and decrease in myosin light chain phosphorylation. Saline infusion can also adversely affect renal hemodynamics. Microperfusion experiments and real-time imaging studies have demonstrated a reduction in renal perfusion and an expansion in kidney volume, compromising O 2 delivery to the renal parenchyma following saline infusion. Clinically, saline infusion for patients post abdominal and cardiovascular surgery is associated with a greater number of adverse effects including more frequent blood product transfusion and bicarbonate therapy, reduced gastric blood flow, delayed recovery of gut function, impaired cardiac contractility in response to inotropes, prolonged hospital stay, and possibly increased mortality. In critically ill patients, saline infusion, compared to balanced fluid infusions, increases the occurrence of acute kidney injury. In summary, saline is a highly acidic fluid. With the exception of saline infusion for patients with hypochloremic metabolic alkalosis and volume depletion due to vomiting or upper gastrointestinal suction, indiscriminate use, especially for acutely ill patients, may cause unnecessary complications and should be avoided. More education regarding saline-related effects and adequate electrolyte management is needed.

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Section: Pathological Effects Of Saline On Renal Hemodynamicsmentioning

confidence: 99%

0.9% saline is neither normal nor physiological

Sun

Yap

et al. 2016

J. Zhejiang Univ. Sci. B

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show abstract

“…This section of the review will try to highlight the important controversies in the area but will not go into exhaustive detail. The interested reader is referred to some excellent reviews, which devote more attention to the subject [8,12,28,95,97,98,[102][103][104][105][106] (plus, see article by Bell et al [107] in this Special Issue). Instead, this review will focus on the critical data leading to the postulate that ATP transduces haemodynamic and tubular information into autoregulatory adjustments in afferent arteriolar diameter by stimulating P2 receptors.…”

Section: P2 Receptors and Their Roles In Renal Autoregulation And Tubmentioning

confidence: 99%

ATP, P2 receptors and the renal microcirculation

Inscho

2009

Purinergic Signalling

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Purinoceptors are rapidly becoming recognised as important regulators of tissue and organ function. Renal expression of P2 receptors is broad and diverse, as reflected by the fact that P2 receptors have been identified in virtually every major tubular/vascular element. While P2 receptor expression by these renal structures is recognised, the physiological functions that they serve remains to be clarified. Renal vascular P2 receptor expression is complex and poorly understood. Evidence suggests that different complements of P2 receptors are expressed by individual renal vascular segments. This unique distribution has given rise to the postulate that P2 receptors are important for renal vascular function, including regulation of preglomerular resistance and autoregulatory behaviour. More recent studies have also uncovered evidence that hypertension reduces renal vascular reactivity to P2 receptor stimulation in concert with compromised autoregulatory capability. This review will consolidate findings related to the role of P2 receptors in regulating renal microvascular function and will present areas of controversy related to the respective roles of ATP and adenosine in autoregulatory resistance adjustments.

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“…As described elsewhere in this Special Issue (see articles by Inscho [33] and Bell et al [37]), there is evidence that ectonucleotidases play a pivotal role in tubuloglomerular feedback (TGF), whereby changes in renal perfusion pressure, or other causes of altered NaCl delivery to the macula densa, ultimately cause compensatory changes in afferent arteriolar resistance so that glomerular filtration rate is regulated [38]. ATP concentrations in renal interstitial fluid increase in response to elevations in renal arterial perfusion pressure [39], and, as indicated above, ATP can act directly on P2X 1 receptors on the afferent arteriole to …”

Section: Tubuloglomerular Feedbackmentioning

confidence: 99%

Ectonucleotidases in the kidney

Shirley

Vekaria

Sévigny

2009

Purinergic Signalling

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Members of all four families of ectonucleotidases, namely ectonucleoside triphosphate diphosphohydrolases (NTPDases), ectonucleotide pyrophosphatase/ phosphodiesterases (NPPs), ecto-5′-nucleotidase and alkaline phosphatases, have been identified in the renal vasculature and/or tubular structures. In rats and mice, NTPDase1, which hydrolyses ATP through to AMP, is prominent throughout most of the renal vasculature and is also present in the thin ascending limb of Henle and medullary collecting duct. NTPDase2 and NTPDase3, which both prefer ATP over ADP as a substrate, are found in most nephron segments beyond the proximal tubule. NPPs catalyse not only the hydrolysis of ATP and ADP, but also of diadenosine polyphosphates. NPP1 has been identified in proximal and distal tubules of the mouse, while NPP3 is expressed in the rat glomerulus and pars recta, but not in more distal segments. Ecto-5′-nucleotidase, which catalyses the conversion of AMP to adenosine, is found in apical membranes of rat proximal convoluted tubule and intercalated cells of the distal nephron, as well as in the peritubular space. Finally, an alkaline phosphatase, which can theoretically catalyse the entire hydrolysis chain from nucleoside triphosphate to nucleoside, has been identified in apical membranes of rat proximal tubules; however, this enzyme exhibits relatively high K m values for adenine nucleotides. Although information on renal ectonucleotidases is still incomplete, the enzymes' varied distribution in the vasculature and along the nephron suggests that they can profoundly influence purinoceptor activity through the hydrolysis, and generation, of agonists of the various purinoceptor subtypes. This review provides an update on renal ectonucleotidases and speculates on the functional significance of these enzymes in terms of glomerular and tubular physiology and pathophysiology.

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ATP as a mediator of macula densa cell signalling

Cited by 57 publications

References 108 publications

0.9% saline is neither normal nor physiological

0.9% saline is neither normal nor physiological

ATP, P2 receptors and the renal microcirculation

Ectonucleotidases in the kidney

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