Stimulation of sodium transport by glucose in the perfused rat kidney

Frega, Norberto; Weinberg, Joel M.; Ross, Brian D.; Leaf, Alexander

doi:10.1152/ajprenal.1977.233.3.f235

Cited by 9 publications

(9 citation statements)

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“…In isolated perfused rat kidneys, addition ofglucose to the perfusion fluid results in an increase in both sodium and water reabsorption (1)(2)(3)(4)(5). In isolated perfused rabbit proximal tubules, glucose added to the luminal fluid, but not to the bath fluid, increases fluid absorption and the transepithelial electrical potential (6).…”

Section: Introductionmentioning

confidence: 99%

Progressive increases in luminal glucose stimulate proximal sodium absorption in normal and diabetic rats.

Bank¹,

Aynedjian²

1990

J. Clin. Invest.

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The effect of progressive increases in intraluminal glucose concentration on proximal tubule sodium absorption was studied in normal and streptozotocin diabetic rats by microperfusion. Each tubule was perfused twice, with and without glucose added to the perfusion fluid. Net sodium and water absorption were markedly enhanced by 300-500 mg% intraluminal glucose in both normal and diabetic rats. Substituting the transported but nonmetabolized glucose analogue, a-methyl D-glucoside for glucose also resulted in marked stimulation of sodium absorption, whereas substituting bicarbonate and acetate for chloride in the perfusion solution inhibited the effect of glucose. These observations suggest that the stimulation of sodium absorption by glucose was mediated by the brush border Na/glucose cotransporter. Sodium concentration and osmolality were found to fall markedly to hypotonic levels when high glucose concentrations were in the perfusion fluid. This luminal hypotonicity may be an important driving force for proximal fluid absorption. In poorly controlled diabetes, high filtered glucose concentrations may lead to enhanced proximal sodium and water absorption, which could in turn contribute to volume expansion, hypertension, and renal hypertrophy. (J. Clin. Invest. 1990. 86:309-316.)

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Section: Introductionmentioning

confidence: 99%

Progressive increases in luminal glucose stimulate proximal sodium absorption in normal and diabetic rats.

Bank¹,

Aynedjian²

1990

J. Clin. Invest.

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“…Both pyruvate and lactate are capable of generating glucose in the in vitro perfused kidney [22]. However, sever al lines of evidence suggest that glycolysis per se does not mediate the beneficial ef fects of these substrates.…”

Section: Discussionmentioning

confidence: 99%

“…However, sever al lines of evidence suggest that glycolysis per se does not mediate the beneficial ef fects of these substrates. First, the concen tration of glucose which appears in the per fusion medium of the in vitro kidney of intact animals as a consequence of gluconeogenesis from lactate or pyruvate is not sufficient by itself to support sodium reab sorption [22], In addition, inhibition of phosphoenol-pyruvate carboxykinase (PEPCK), a key step in gluconeogenesis from pyruvate and lactate, with 3-mercaptopicolinate, does not prevent the ability of pyruvate and lac tate to support sodium reabsorption [22]. In the toad bladder, iodoacetate blocks the stimulatory effect of aldosterone on sodium transport and this inhibition can be reversed with pyruvate [21].…”

Section: Discussionmentioning

confidence: 99%

Aldosterone Effects on Renal Function in the Isolated Perfused Rat Kidney

Solomon¹,

Silva²,

Epstein³

1979

Kidney Blood Press Res

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The excretion of potassium and the reabsorption of sodium were studied in isolated perfused kidneys of adrenalectomized rats following the administration of aldosterone. Aldosterone (10^-7M) produced a rapid increase in fractional excretion of potassium, without affecting glomerular filtration rate, urine flow rate or sodium reabsorption. Spironolactone (10^-4M) completely abolished the kaliuretic effect of aldosterone, while actinomycin D had no inhibitory effect. In the absence of exogenous metabolic substrate, enhancement of potassium excretion was not seen following aldosterone. With either glucose, pyruvate, lactate or α-ketoglutarate in the perfusion medium, the kaliuretic effect of aldosterone was restored. The results confirm the direct action of aldosterone on renal potassium excretion and its dependency upon the availability of specific metabolic substrates.

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“…Neither the effect of the other substrates nor the effect of the duration of per fusion was taken into consideration. Conse quently, it is difficult to draw, from those ex periments [26], firm conclusions regarding the effect of glucose per se on % TNa.…”

Section: Relation To Renal Functionmentioning

confidence: 98%

“…This ef fect would be unrelated to the energy derived from glucose Ql>x, since we found no correla tion between Qox and % TNa. It should be noted that unlike previous studies in the IPRK [11,26] the effect of increasing oncotic pressure on %TNa (and GFR) was circumvented in the pre sent study (COP clamp, see Methods) in order to better assess the effect of glucose on % TN., and GFR in relation to the duration of perfu sion. In the study by Frega et al [26], the experiment consisted of a control period in the presence of 2.5 mmol/1 butyrate (plus albuminbound fatty acids), and an experimental period which followed the addition of glucose (2.5-5.0 mmol/1).…”

Section: Relation To Renal Functionmentioning

confidence: 99%

Kinetics of Glucose Decarboxylation in the Substrate-Limited Isolated Perfused Kidney

Anaizi¹,

Cohen²

1991

Kidney Blood Press Res

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Rat kidneys were perfused with a cell-free perfusate containing substrate-free albumin, different glucose concentrations (0.20–5.0 mmol/l), and uniformly labeled ¹⁴C-glucose. The rate of glucose decarboxylation (Q_ox), as a function of [glucose]_p, displayed saturation kinetics [V_max = 0.35 µmol/(g · min); K_m = 0.87mmol/l]; saturation occurred at [glucose]_p = 1.0–2.0mmol/l. Although the presence of as low as 0.2mmol/l of glucose significantly increased fractional sodium reabsorption (%T_Na), there was no correlation between [glucose]_p or Q_ox and %T_Na. However, free water clearance (C_H2O or C_H2O/GFR) was directly proportional to [glucose]_pand independent of Q_ox. We conclude that (1) in the absence of other substrates, renal glucose Q_oxsaturates at hypoglycemic levels of glucose and (2) glucose plays an important role in the generation of solute-free water, a role that is unrelated to glucose Q_ox.

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Stimulation of sodium transport by glucose in the perfused rat kidney

Cited by 9 publications

References 0 publications

Progressive increases in luminal glucose stimulate proximal sodium absorption in normal and diabetic rats.

Progressive increases in luminal glucose stimulate proximal sodium absorption in normal and diabetic rats.

Aldosterone Effects on Renal Function in the Isolated Perfused Rat Kidney

Kinetics of Glucose Decarboxylation in the Substrate-Limited Isolated Perfused Kidney

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