Dipyridamole decreases glomerular filtration in the sodium-depleted dog. Evidence for mediation by intrarenal adenosine.

Arend, Lois J.; Thompson, Carl I.; Spielman, William S.

doi:10.1161/01.res.56.2.242

Cited by 46 publications

(16 citation statements)

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“…In rats and dogs, the kidney is rendered insensitive to the vasoconstrictive action of adenosine at conditions of a high NaCl diet and volume expansion when plasma renin activity is low (11,249,252,254). Correspondingly, high renin states of the animal are associated with an increased potency of adenosine to induce vasoconstriction and to lower GFR (249,252,254).…”

Section: Dietary Nacl Status and Renin-angiotensin Systemmentioning

confidence: 99%

“…Adenosine may contribute to signal transduction in TGF because it reduces glomerular capillary pressure and SNGFR by predominant afferent arteriolar vasoconstriction and because this response is rapid in onset and short in duration when the adenosine delivery is discontinued (11,103,133,228,244,249,251,255,289,298). Table 3 summarizes the interactions between different conditions and factors and the renal vasoconstriction mediated by adenosine as well as TGF activity.…”

Section: B Altering Tgf Responses By Manipulating Adenosine Receptormentioning

confidence: 99%

“…Evidence for an inhibitory action of endogenous adenosine on renin secretion was provided by experiments in which renal adenosine concentrations were elevated by administration of the adenosine reuptake inhibitor dipyridamole (11,324) or by ATP depletion using maleic acid (10). Most notably, a single application of the adenosine A 1 receptor antagonist FK-453 was found to increase plasma renin concentrations in humans (15), indicating a tonic inhibition of renin secretion by adenosine A 1 receptor activation.…”

Section: B Role Of Endogenous Adenosine In the Control Of Renin Releasementioning

confidence: 99%

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Adenosine and Kidney Function

Vallon

Mühlbauer²,

Oßwald³

2006

Physiological Reviews

401

379

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In this review we outline the unique effects of the autacoid adenosine in the kidney. Adenosine is present in the cytosol of renal cells and in the extracellular space of normoxic kidneys. Extracellular adenosine can derive from cellular adenosine release or extracellular breakdown of ATP, AMP, or cAMP. It is generated at enhanced rates when tubular NaCl reabsorption and thus transport work increase or when hypoxia is induced. Extracellular adenosine acts on adenosine receptor subtypes in the cell membranes to affect vascular and tubular functions. Adenosine lowers glomerular filtration rate (GFR) by constricting afferent arterioles, especially in superficial nephrons, and acts as a mediator of the tubuloglomerular feedback, i.e., a mechanism that coordinates GFR and tubular transport. In contrast, it leads to vasodilation in deep cortex and medulla. Moreover, adenosine tonically inhibits the renal release of renin and stimulates NaCl transport in the cortical proximal tubule but inhibits it in medullary segments including the medullary thick ascending limb. These differential effects of adenosine are subsequently analyzed in a more integrative way in the context of intrarenal metabolic regulation of kidney function, and potential pathophysiological consequences are outlined.

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Section: Dietary Nacl Status and Renin-angiotensin Systemmentioning

confidence: 99%

Section: B Altering Tgf Responses By Manipulating Adenosine Receptormentioning

confidence: 99%

Section: B Role Of Endogenous Adenosine In the Control Of Renin Releasementioning

confidence: 99%

See 1 more Smart Citation

Adenosine and Kidney Function

Vallon

Mühlbauer²,

Oßwald³

2006

Physiological Reviews

401

379

View full text Add to dashboard Cite

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“…For this reason it is normally unlikely that adenosine would ever reach sufficient concentration in blood to act as a blood-borne mediator transferring information from one organ to another. However, during situations in which adenosine uptake is pharmacologically Downloaded from http://ahajournals.org by on April 3, 2019 inhibited with nucleoside transport inhibitors (e.g., dipyridamole, papaverine), plasma levels of adenosine may be markedly elevated, 16 affecting function in multiple organs.…”

Section: Schematic Representation Summarizing the Localization Of Ectmentioning

confidence: 99%

Adenosine receptors and signaling in the kidney.

1991

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It is now generally accepted that adenosine is capable of regulating a wide range of physiological functions. Nowhere is the diversity of this action better illustrated than in the kidney. When adenosine binds to plasma membrane receptors on a variety of cell types in the kidney, it stimulates functional responses that span the entire spectrum of renal physiology, including alterations in hemodynamics, hormone and neurotransmitter release, and tubular reabsorption. These responses to adenosine appear to represent a means by which the organ and its constituent cell types can regulate their metabolic demand such that it is maintained at an appropriate level for the prevailing metabolic supply. Extracellular adenosine, produced from the hydrolysis of adenosine 5'-monophosphate and stimulated by increased substrate availability and enzyme induction, acts on at least two types of cell surface receptors to stimulate or inhibit the production of cyclic adenosine-3',5'-monophosphate and also acts in some renal cells to stimulate the production of inositol phosphates and elevation of cytosolic calcium concentration. To understand when and why this complicated system becomes activated, how it interacts with other known extracellular effector systems, and ultimately how to manipulate the system to therapeutic advantage by selective agonists or antagonists, requires a detailed knowledge of renal adenosine receptors and their signaling mechanisms. The following discussion attempts to highlight our knowledge in this area, to present a modified hypothesis for adenosine as a feedback regulator of renal function, and to identify some important questions regarding the specific cellular mechanisms of adenosine in renal cell types. T he kidney, like many organs, is endowed with intrinsic mechanisms that allow it to self-regulate many of its functions. Two well-known examples are the relatively constant glomerular filtration rate (GFR) and renal blood flow over a wide range of arterial pressure (i.e., autoregulation) and the ability to release renin in response to changes in renal perfusion pressure independent of neural or humoral signals. It was the search to understand the renal mechanism responsible for this intrinsic regulation that prompted investigators to turn their interest toward adenosine. Previous reviews 1 -5 have dealt specifically with a proposed role for adenosine in the control of GFR and renin release. Although this may have prompted much of the original interest in intrarenal adenosine, recent investigations have revealed adenosine to have a much broader regulatory role. The present discussion focuses From the Departments of Physiology and Biochemistry, Michigan State University, East Lansing, Mich.

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“…In young spontaneously hypertensive rats (SHR), TGF activity is augmented compared to that in age-matched Wistar Kyoto rats, suggesting that it may participate in the initiation and/or nephrotic patients (9) via mechanisms that involve preservation of the charge barrier of the glomerulus (6)(7)(8) and reduction in GFR (6,9). Dipyridamole has been shown to decrease GFR in dogs (10) and humans (9,11). This decrease in GFR, which in humans was accompanied by a fall in filtration fraction (FF) (9), seems to indicate a reduction in intraglomerular pressure via the vasodilatation of postglomerular efferent arterioles.…”

Section: Introductionmentioning

confidence: 99%