Interplay between renal endothelin and purinergic signaling systems

Gohar, Eman Y.; Kasztan, Małgorzata; Pollock, David M.

doi:10.1152/ajprenal.00639.2016

Cited by 8 publications

(6 citation statements)

References 35 publications

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“…Previous studies in our laboratory revealed that angiotensin II could induce a rapid release of ATP in the isolated kidney, a response that was strongly enhanced in Dahl salt‐sensitive rats fed a high‐salt diet . Another mechanism that may stimulate ATP release and sodium excretion in response to an increase of RPP could be the proposed crosstalk between purinergic and endothelin signaling . Consistent with this, ATP release and P2 receptor stimulation were shown to be upstream events of the flow‐induced increases in endothelin expression and activity in the CCDs both of which play significant roles in the regulation of ENaC activity …”

Section: Discussionsupporting

confidence: 69%

Acute In Vivo Analysis of ATP Release in Rat Kidneys in Response to Changes of Renal Perfusion Pressure

Palygin

Evans

Cowley

et al. 2017

JAHA

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BackgroundATP and derivatives are recognized to be essential agents of paracrine signaling. It was reported that ATP is an important regulator of the pressure‐natriuresis mechanism. Information on the sources of ATP, the mechanisms of its release, and its relationship to blood pressure has been limited by the inability to precisely measure dynamic changes in intrarenal ATP levels in vivo.Methods and ResultsNewly developed amperometric biosensors were used to assess alterations in cortical ATP concentrations in response to changes in renal perfusion pressure (RPP) in anesthetized Sprague–Dawley rats. RPP was monitored via the carotid artery; ligations around the celiac/superior mesenteric arteries and the distal aorta were used for manipulation of RPP. Biosensors were acutely implanted in the renal cortex for assessment of ATP. Rise of RPP activated diuresis/natriuresis processes, which were associated with elevated ATP. The increases in cortical ATP concentrations were in the physiological range (1–3 μmol/L) and would be capable of activating most of the purinergic receptors. There was a linear correlation with every 1‐mm Hg rise in RPP resulting in a 70‐nmol/L increase in ATP. Furthermore, this elevation of RPP was accompanied by a 2.5‐fold increase in urinary H2O2.ConclusionsChanges in RPP directly correlate with renal sodium excretion and the elevation of cortical ATP. Given the known effects of ATP on regulation of glomerular filtration and tubular transport, the data support a role for ATP release in the rapid natriuretic responses to acute increases in RPP.

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Section: Discussionsupporting

confidence: 69%

Acute In Vivo Analysis of ATP Release in Rat Kidneys in Response to Changes of Renal Perfusion Pressure

Palygin

Evans

Cowley

et al. 2017

JAHA

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“…Consequently, P2 receptor-dependent effects in the upstream vasculature could have profound effects on renal medullary hemodynamics and tubular function. Intramedullary infusion of UTP can increase sodium excretion, possibly by activating P2Y 2/4 receptors (171,172). This natriuretic response was prevented by P2 receptor blockade with suramin, or by combined endothelin A/endothelin B receptor blockade, suggesting a novel endothelin and P2 receptor interaction (see sects.…”

Section: Extracellular Nucleotides/p2 Receptors and Medullary Blood Flowmentioning

confidence: 96%

Extracellular Nucleotides and P2 Receptors in Renal Function

Vallon

Unwin

Inscho

et al. 2020

Physiological Reviews

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The understanding of the nucleotide/P2 receptor system in the regulation of renal hemodynamics and transport function has grown exponentially over the last 20 yr. This review attempts to integrate the available data while also identifying areas of missing information. First, the determinants of nucleotide concentrations in the interstitial and tubular fluids of the kidney are described, including mechanisms of cellular release of nucleotides and their extracellular breakdown. Then the renal cell membrane expression of P2X and P2Y receptors is discussed in the context of their effects on renal vascular and tubular functions. Attention is paid to effects on the cortical vasculature and intraglomerular structures, autoregulation of renal blood flow, tubuloglomerular feedback, and the control of medullary blood flow. The role of the nucleotide/P2 receptor system in the autocrine/paracrine regulation of sodium and fluid transport in the tubular and collecting duct system is outlined together with its role in integrative sodium and fluid homeostasis and blood pressure control. The final section summarizes the rapidly growing evidence indicating a prominent role of the extracellular nucleotide/P2 receptor system in the pathophysiology of the kidney and aims to identify potential therapeutic opportunities, including hypertension, lithium-induced nephropathy, polycystic kidney disease, and kidney inflammation. We are only beginning to unravel the distinct physiological and pathophysiological influences of the extracellular nucleotide/P2 receptor system and the associated therapeutic perspectives.

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“…Via the A1 receptor, adenosine plays a critical role in constricting the afferent arteriole as part of the tubuloglomerular feedback (TGF) system (57). The integrative nature of renal regulatory systems is a fundamental tenet of renal physiologists and includes, among other examples, the intersection of renal purinergic and endothelin systems and their effects on sodium excretion (58). Endothelin is a vasoconstrictor involved in regulating renal blood flow and sodium transport (59,60).…”

Section: Introductionmentioning

confidence: 99%

Induction of renal tumor necrosis factor-α and other autacoids and the beneficial effects of hypertonic saline in acute decompensated heart failure

Gatzoflias

Hao

Ferreri

2021

American Journal of Physiology-Renal Physiology

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While administration of Hypertonic Saline (HSS) in combination with diuretics has yielded improved weight loss, preservation of renal function, and reduction in hospitalization time in the clinical setting of patients with acute decompensated heart failure (ADHF), the mechanisms that underlie these beneficial effects remain unclear and additional studies are needed before this approach can be adopted on a more consistent basis. As high salt conditions stimulate production of several renal autacoids that exhibit natriuretic effects, renal physiologists can contribute to the understanding of mechanisms by which HSS leads to increased diuresis both as an individual therapy, as well as in combination with loop diuretics. For instance, since HSS increases TNF-α production by proximal tubule (PT) and thick ascending limb of Henle's loop (TAL) epithelial cells, this 'Perspective article' is aimed at highlighting how the effects of TNF-α produced by these cell types may contribute to the beneficial effects of HSS in patients with ADHF. While TNF-α produced by infiltrating macrophages and T cells exacerbate and attenuate renal damage, respectively, production of this cytokine within the tubular compartment of the kidney functions as an intrinsic regulator of blood pressure and sodium homeostasis via mechanisms along the nephron related to inhibition of NKCC2 activity and angiotensinogen (AGT) expression. Thus, in the clinical setting of ADHF and hyponatremia, induction of TNF-α production along the nephron by administration of HSS may attenuate NKCC2 activity and AGT expression as part of a mechanism that prevents excessive Na+ reabsorption in the TAL, thereby mitigating volume overload.

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Interplay between renal endothelin and purinergic signaling systems

Cited by 8 publications

References 35 publications

Acute In Vivo Analysis of ATP Release in Rat Kidneys in Response to Changes of Renal Perfusion Pressure

Acute In Vivo Analysis of ATP Release in Rat Kidneys in Response to Changes of Renal Perfusion Pressure

Extracellular Nucleotides and P2 Receptors in Renal Function

Induction of renal tumor necrosis factor-α and other autacoids and the beneficial effects of hypertonic saline in acute decompensated heart failure

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