Stoichiometry and coupling of active transport to oxidative metabolism in epithelial tissues

Mandel, Lazaro J.; Balaban, Robert S.

doi:10.1152/ajprenal.1981.240.5.f357

Cited by 90 publications

(104 citation statements)

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“…Another possible mechanism for the lack of HCO-stimulation of apical Cl-/base exchange is enhanced cellular acid loading due to an increase in lactic acid production in HCO -. However, since in the proximal tubule metabolic ATP production is coupled to ATP used primarily by the basolateral Na'-K+-ATPase (48), it is likely that in Na+-free solutions metabolic proton production was low. In addition, a previous study in rabbit proximal tubules has documented a greater rate of glycolytic lactate production in Hepes than in HCO--containing solutions (49).…”

Section: Discussionmentioning

confidence: 99%

Mechanism of apical and basolateral Na(+)-independent Cl-/base exchange in the rabbit superficial proximal straight tubule.

Kurtz

Nagami²,

Yanagawa³

et al. 1994

J. Clin. Invest.

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The present study was undertaken to determine the magnitude and mechanism of base transport via the apical and basolateral Na '-independent Cl -/base exchangers in rabbit isolated perfused superficial S2 proximal tubules. The results demonstrate that there is an apical Na '-independent Cl-/ base exchanger on both membranes. HCO3 fails to stimulate apical Cl-/base exchange in contrast to the basolateral exchanger. Inhibition of endogenous HCO3 production does not alter the rate of apical Cl-/base exchange in Hepesbuffered solutions. Both exchangers are inhibited by H2DIDS and furosemide; however, the basolateral anion exchanger is more sensitive to these inhibitors. The results indicate that the apical and basolateral Cl-/base exchangers differ in their transport properties and are able to transport base equivalents in the absence of formate. The formate concentration in rabbit arterial serum is -6 ,uM and in vitro tubule formate production is < 0.6 pmol/min per mm.Formate in the micromolar range stimulates Jv in a dosedependent manner in the absence of a transepithelial Na+ and Cl-gradient and without a measurable effect on Cl--induced equivalent base flux. Apical formic acid recycling cannot be an important component of any cell model, which accounts for formic acid stimulation of transcellular NaCl transport in the rabbit superficial S2 proximal tubule. We propose that transcellular NaCl transport in this nephron segment is mediated by an apical Na+/H+ exchanger in parallel with a Cl-/OH-exchanger and that the secreted H+ and OH -ions form H20 in the tubule lumen. (J. Clin. Invest. 1994. 94:173-183.) Key words: Na+/H+ exchange-

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Section: Discussionmentioning

confidence: 99%

Mechanism of apical and basolateral Na(+)-independent Cl-/base exchange in the rabbit superficial proximal straight tubule.

Kurtz

Nagami²,

Yanagawa³

et al. 1994

J. Clin. Invest.

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“…Experiments involving manipulation of rates of Na + transport yield a positive, linear relationship between transport and O 2 consumption rates, and such results have been used to calculate the ATP cost of Na + pumping by Na + -K + -ATPase (Mandel and Balaban, 1981). Although control analysis has not been conducted on perfused kidneys or kidney tubules in vitro, it is apparent that the metabolic rates of kidneys are controlled by rates of energy expenditure, i.e.…”

Section: Cellular Energy Metabolism: Lessons From Control Analysismentioning

confidence: 99%

Multi-level regulation and metabolic scaling

Suarez

Darveau

2005

Journal of Experimental Biology

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Metabolic rates scale allometrically, such that a unit mass of elephant has a metabolic rate much less than that of a unit mass of mouse. To empiricists, the question 'what causes the allometric scaling of metabolic rates?' is one that is inextricably linked to the question 'what determines metabolic rates?' This is because whatever phenomena determine metabolic rates should presumably play major roles in driving their allometric scaling. The fundamental importance of both questions has been recognized by biologists for a century, and studies addressing them have had long and illustrious histories. Introductions to the phenomenon of metabolic scaling and accounts of the historical development of ideas and studies devoted to the subject can be found in excellent books (Calder, 1984;Schmidt-Nielsen, 1984) and reviews (Calder, 1981;Hoppeler et al., 1980;Porter, 2001;Taylor, 1987;Weibel, 1987) and are beyond the scope of this article. Here, we discuss some empirical data from the literature of comparative physiology to address the issue of what determines metabolic rates in animals. We relate this information to the allometric scaling of metabolic rates and comment on recently proposed models for metabolic scaling. Animals as the sum of their partsWhen data for basal metabolic rate, BMR, are plotted against body mass, M b , on logarithmic coordinates, the slope of the linear relationship, referred to as the allometric exponent, b, in the equation:is significantly less than 1.0, where a is the vertical intercept (Schmidt-Nielsen, 1984 Metabolic control analysis has revealed that flux through pathways is the consequence of system properties, i.e. shared control by multiple steps, as well as the kinetic effects of various pathways and processes over each other. This implies that the allometric scaling of flux rates must be understood in terms of properties that pertain to the regulation of flux rates. In contrast, proponents of models considering the scaling of branching or fractal-like systems suggest that supply rates determine metabolic rates. Therefore, the allometric scaling of supply alone provides a sufficient explanation for the allometric scaling of metabolism. Examination of empirical data from the literature of comparative physiology reveals that basal metabolic rates (BMR) are driven by rates of energy expenditure within internal organs and that the allometric scaling of BMR can be understood in terms of the scaling of the masses and metabolic rates of internal organs. Organ metabolic rates represent the sum of tissue metabolic rates while, within tissues, cellular metabolic rates are the outcome of shared regulation by multiple processes. Maximal metabolic rates (MMR, measured as maximum rates of O 2 consumption, V O ∑ max ) during exercise also scale allometrically, are also subject to control by multiple processes, but are due mainly to O 2 consumption by locomotory muscles. Thus, analyses of the scaling of MMR must consider the scaling of both muscle mass and muscle energy expenditure. Consistent with t...

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“…This energy consumption is disproportionate for the size of the tissue (about 6% of body mass in these studies). Accordingly, the coupling of active transport to oxidative metabolism in epithelial tissues (Zerahn, 1956;Mandel and Balaban, 1981) suggests that the GI tract likely elicits an even greater SDA response, relative to its mass, than that of the whole animal, although investigations of postprandial oxygen consumption by isolated intestinal epithelia are scant. The importance of the marine fish intestine in osmoregulation suggests the baseline (i.e.…”

Section: Introductionmentioning

confidence: 99%

The intestinal response to feeding in seawater gulf toadfish, Opsanus beta, includes elevated base secretion and increased epithelial oxygen consumption

Taylor

Grosell

2009

Journal of Experimental Biology

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Stoichiometry and coupling of active transport to oxidative metabolism in epithelial tissues

Cited by 90 publications

References 0 publications

Mechanism of apical and basolateral Na(+)-independent Cl-/base exchange in the rabbit superficial proximal straight tubule.

Mechanism of apical and basolateral Na(+)-independent Cl-/base exchange in the rabbit superficial proximal straight tubule.

Multi-level regulation and metabolic scaling

The intestinal response to feeding in seawater gulf toadfish, Opsanus beta, includes elevated base secretion and increased epithelial oxygen consumption

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