Adenosinetriphosphate in rat renal papilla: effects of vasopressin and of ischemia

Nf, Jones; Welt, Louis G.

doi:10.1152/ajplegacy.1967.212.4.939

Cited by 18 publications

(16 citation statements)

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“…ATP values at 30, 60 and 300 s of ischemia were significantly dif ferent from zero time values. The data with respect to ATP are in general agreement with those of Jones and Welt [7] in the rat kidney. The present study shows that changes in papillary ADP and AMP were also different from those occurring in either cortex or red medulla.…”

Section: Ischemia Controlsupporting

confidence: 89%

“…to the extent that ATP con tinues to be used, on the concentration of ATP. [7] and Needleman et al [17] found that ischemia led to a rapid and large decline in renal cortical ATP content and a slower and smaller decrease in medul lary and papillary ATP. The more rapid decrease in cortical ATP supports observa tions that the cortex requires oxygen to pro duce ATP and carry out active transport while medullary and papillary tissue have anaerobic capacity to do so [8,12,16].…”

Section: Introductionmentioning

confidence: 99%

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Effect of Ischemia and Hypertonic Saline Loading on Renal Adenine Nucleotides

Urbaitis¹

1984

Kidney Blood Press Res

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The present study was done to determine: (1) regional (cortex, red medulla and papilla) changes in ATP, ADP and AMP resulting from periods of ischemia of 30-300 s; (2) whether ischemic changes in adenine nucleotides or lactate were modified by hypertonic saline loading, and (3) whether adenylate kinase activity was present in each region. Ischemia led to changes in all three adenine nucleotides which were characteristic for each region. In cortex, there was a major decrease in ATP, increase in AMP and a small transient increase in ADP. In red medulla there were slower changes in ATP, ADP and AMP. In papilla, ATP decreased slightly and ADP, as opposed to AMP, accumulated. Hypertonic saline loading increased the rate of ATP decrease and AMP accumulation, most markedly in red medulla. Lactate concentration rose similarly in control and hypertonic saline studies. Adenylate kinase activity was found to be present in each region. In conclusion: (1) the rate of change of all three adenine nucleotides differs among the three renal areas studied; (2) increases in renal transport work, associated with hypertonic saline loading, are reflected in an increase in the rate of ATP decay during ischemia; (3) anaerobic metabolism, as indicated by tissue lactate concentration, is not altered by hypertonic saline loading, and (4) the failure of AMP to accumulate in papilla is not due to the absence of adenylate kinase.

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Section: Ischemia Controlsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Effect of Ischemia and Hypertonic Saline Loading on Renal Adenine Nucleotides

Urbaitis¹

1984

Kidney Blood Press Res

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“…GFR (6,38), and this feature is likely due to the short delay in freezing the tissue (38 (39). Close correlation between the decrease in Pi uptake by BBM and the increase in UpiV, consequent to NiAm treatment (Fig.…”

Section: Discussionmentioning

confidence: 85%

Possible role of nicotinamide adenine dinucleotide as an intracellular regulator of renal transport of phosphate in the rat.

Kempson¹,

Colón‐Otero²,

Ou³

et al. 1981

J. Clin. Invest.

120

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A B S T R A C T In these experiments we investigated whether NAD could serve as an intracellular modulator of the brush border membrane (BBM) transport of inorganic phosphate (Pi). NAD, both oxidized (NAD+) and reduced (NADH) form, inhibited the Na+-dependent uptake of 32Pi in the concentration range of 10-300 zM NAD when added in vitro to BBM vesicles isolated from rat kidney cortex, but did not inhibit BBM uptake of D-[3H]glucose or BBM uptake of 22Na+. Neither nicotinamide (NiAm) nor adenosine alone influenced BBM uptake of 32Pi. NAD had a similar relative effect (percent inhibition) in BBM from rats stabilized on low Pi diet (0.07% Pi), high Pi diet (1.2% Pi), or normal Pi diet (0.7% Pi).Subsequently, we examined the renal effects of changing the tissue NAD level in vivo. Rats stabilized on low Pi diet were injected intraperitoneally with NiAm (0.25-1.0 g/kg body wt); urinary excretions of Pi (UpV), of fluid, and of other solutes were measured before and after NiAm injection, then renal cortical tissue nucleotide content was determined, and a BBM fraction was isolated for transport measurements. In BBM from NiAm-treated rats, the Na+-dependent uptake of 32Pi was decreased, but BBM uptake of D-[3H]glucose and BBM uptake of22Na+ were not changed. NiAm 29 December 1980. mum change, 290%), a lesser increase in NADH (maximum change, +45%), but no change in the content of ATP or cyclic AMP in the renal cortex. Na+-dependent BBM uptake of 32Pi was inversely correlated with NAD+ content in renal cortex (r = -0.77+0.1; P < 0.001) arid with UpiV (r = -0.67+0.13; P < 0.01). NAD+ in renal cortex was positively correlated with UpjV (r = 0.88±0.05; P < 0.001). Injection of NiAm elicited a marked increase in Up1V, but no change in excretions of creatinine or K+, or in urine flow; excretion of Na+ and Ca declined. NiAm injection caused similar renal responses, in normal and in thyroparathyroidectomized rats, as well as in rats on normal Pi diet and low Pi diet.We conclude that NAD can serve as an intracellular modulator (inhibitor) of Na+-dependent transport of Pi across the renal luminal BBM and across the proximal tubular wall by its direct interaction with BBM. We propose that at least some hormonal and/or metabolic stimuli elicit phosphaturia by increasing NAD+ in cytoplasm of proximal tubular cells. INTRODUCTIONA Na+-dependent Pi uptake by the luminal brush border membrane (BBM) and its regulation by various hormonal and metabolic stimuli (1-3) are initial and perhaps quantitatively determining cellular steps in proximal tubular reabsorption of phosphate (Pi). Parathyroid hormone (PTH) or vitamin D (1, 3) has been reported to decrease BBM uptake ofPi, whereas growth hormone reportedly has an opposite effect (4). In phosphaturia associated with starvation (5) or a high Pi diet (2), the capacity of the BBM to transport Pi is diminished; feeding with a diet selectively deficient in Pi, however, leads to a marked increase in BBM uptake of Pi (1)(2)(3)5), which is apparently independent of the J. Clin. (5, 16). HPD ...

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“…The rate of oxygen consumption by the kidney is high [1] and it is generally accepted that most of the active transport by the kidney is supported by oxidative metab olism through the generation of ATP [2], Previous investigators have found the ATP concentration in the kidney to be between 0.7 and 2.1 pmol/g wet weight depending upon the species and method of analysis [3][4][5][6][7][8][9][10][11][12], However, whole tissue concentra tions reflect the balance between production and utilization of ATP and provide no infor mation concerning the absolute rates of turnover.…”

Section: Introductionmentioning

confidence: 99%

“…Furthermore, whole kidney (which includes the anaerobi cally glycolytic inner medulla) metabolite concentrations were measured. Jones and Welt [4] demonstrated that medullary ATP concentrations are maintained during isch emia; thus, whole kidney values may not represent the changes occurring in cortex.…”

Section: Introductionmentioning

confidence: 99%

Effects of Ischemia on Metabolite Concentrations in Dog Renal Cortex

Cunarro¹,

Schultz²,

Johnson³

et al. 1982

Kidney Blood Press Res

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To investigate the effects of ischemia on renal metabolites, sequential slices of renal cortex were removed during 5 min of renal artery occlusion and for 5 min after release of occlusion. ATP concentrations rapidly fell during ischemia and rose during the post-ischemic period. Based on the rate of decline of ATP concentrations, the rate of ATP production was estimated to be 0.5 µ mol ATP/g/min. This is considerably less than the rate of ATP production estimated from renal O₂ consumption. During ischemia, AMP concentrations rose, confirming the activity of adenylate kinase. The control lactate/pyruvate ratio suggested that dog kidney cytosol is more reduced than the cytosol of rat liver and kidney. During ischemia, the lactate concentrations and the lactate/pyruvate ratio of dog renal cortex increased as expected, and fell after restoration of blood flow. β-Hydroxybutyrate concentrations were considerably lower than those previously reported for rat liver and kidney. The β-hydroxybutyrate/acetoacetate ratio was not measurable during ischemia. However, the mitochondrial redox state, calculated from the glutamate/α-ketoglutarate·NH⁺₄ ratio, was similar to previous reports and this ratio appropriately changed during the ischemic and post-ischemic period.

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Adenosinetriphosphate in rat renal papilla: effects of vasopressin and of ischemia

Cited by 18 publications

References 0 publications

Effect of Ischemia and Hypertonic Saline Loading on Renal Adenine Nucleotides

Effect of Ischemia and Hypertonic Saline Loading on Renal Adenine Nucleotides

Possible role of nicotinamide adenine dinucleotide as an intracellular regulator of renal transport of phosphate in the rat.

Effects of Ischemia on Metabolite Concentrations in Dog Renal Cortex

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