Proton compartmentation in rat renal cortical tubules

1989 ◽  
Vol 256 (6) ◽  
pp. F986-F993 ◽  
Author(s):  
A. C. Schoolwerth ◽  
F. A. Gesek ◽  
R. M. Culpepper

To study the control of renal ammoniagenesis, a technique was developed to estimate simultaneously intracellular (pHi) and intramitochondrial (pHm) pH in suspensions of rat renal cortical tubules. pHi was estimated with the fluorescent probe 2',7'biscarboxyethyl-5(6)-carboxy-fluorescein (BCECF). The intracellular distribution of the weak acid 5,5-dimethyloxazolidine-2,4-dione (DMO) allowed calculation of pHm with the use of values of pHi obtained with BCECF and tubule mitochondrial content. At medium pH (pHe) 7.4, pHi was 7.08 +/- 0.02. Over the pHe range 7.0-7.7, pHi was linearly related to pHe, but the pH gradient across the cell membrane decreased as pHe was lowered. No difference in the relationship between pHe and pHi was obtained when tubules were incubated in the presence of a nonbicarbonate or bicarbonate-buffered medium. Changes in pHe with bicarbonate-buffered media resulted in identical pHi values, whether the changes were induced by altered bicarbonate or CO2 content. At pHe 7.4, pHm was 7.78 +/- 0.6 in bicarbonate-buffered medium but was higher (0.2-0.3 pH units) when tubules were bathed in nonbicarbonate-buffered medium. pHm was linearly related to pHi in either buffer. The pH gradient across the inner mitochondrial membrane was also positively correlated with pHe. The present studies indicate the suitability of the techniques for estimating pHi and pHm simultaneously in suspensions of rat renal cortical tubules. Parallel changes occur in both intracellular compartments when pHe is altered. pHm, which is approximately 0.7 pH units greater than pHi, decreases in acute acidosis. This decrease may be important in stimulating renal ammoniagenesis, possibly by activation of alpha-ketoglutarate dehydrogenase.

2016 ◽  
Vol 39 (5) ◽  
pp. 2014-2024 ◽  
Author(s):  
Mariela Arias-Hidalgo ◽  
Jan Hegermann ◽  
Georgios Tsiavaliaris ◽  
Fabrizio Carta ◽  
Claudiu T. Supuran ◽  
...  

Background/Aims: Across the mitochondrial membrane an exceptionally intense exchange of O2 and CO2 occurs. We have asked, 1) whether the CO2 permeability, PM,CO2, of this membrane is also exceptionally high, and 2) whether the mitochondrial membrane is sufficiently permeable to HCO3- to make passage of this ion an alternative pathway for exit of metabolically produced CO2. Methods: The two permeabilities were measured using the previously published mass spectrometric 18O exchange technique to study suspensions of mitochondria freshly isolated from rat livers. The mitochondria were functionally and morphologically in excellent condition. Results: The intramitochondrial CA activity was exclusively localized in the matrix. PM,CO2 of the inner mitochondrial membrane was 0.33 (SD ± 0.03) cm/s, which is the highest value reported for any biological membrane, even two times higher than PM,CO2 of the red cell membrane. PM,HCO3- was 2· 10-6 (SD ± 2· 10-6) cm/s and thus extremely low, almost 3 orders of magnitude lower than PM,HCO3- of the red cell membrane. Conclusion: The inner mitochondrial membrane is almost impermeable to HCO3- but extremely permeable to CO2. Since gas channels are absent, this membrane constitutes a unique example of a membrane of very high gas permeability due to its extremely low content of cholesterol.


1981 ◽  
Vol 196 (1) ◽  
pp. 133-147 ◽  
Author(s):  
R J Davis ◽  
M D Brand ◽  
B R Martin

1. A recently developed technique for the measurement of plasma-membrane and mitochondrial-membrane potentials in intact cells by using the distribution of 86Rb+ and [3H]methyltriphenylphosphonium+ has enabled us to characterize a novel insulin effect on fat-cell mitochondria. For control cells the plasma-membrane and mitochondrial-membrane potentials were 75 mV and 152 mV respectively. Insulin (10 mu units/ml) caused a 9 mV hyperpolarization of the plasma membrane and a 19 mV depolarization of the mitochondrial membrane. 2. The insulin-dependent mitochondrial depolarization was observed at physiological insulin concentrations (10 mu units/ml) and was apparent when the cells metabolized a wide variety of substrates. 3. Evidence from the uptake of the weak acid 5,5-dimethyloxazolidine-2,4-dione by fat-cells was interpreted as indicating that the mitochondrial pH gradient was increased by insulin. 4. Insulin alters the balance between the electrical and pH-gradient components that form the mitochondrial protonmotive force. A model is proposed.


1991 ◽  
Vol 261 (3) ◽  
pp. R719-R726 ◽  
Author(s):  
S. Abrahams ◽  
L. Greenwald ◽  
D. L. Stetson

In mammals, the length of the loops of Henle increases with increasing body size without a concomitant rise in urinary concentrating ability. Because mass-specific metabolic rate falls with increasing body mass, this study sought to determine the extent to which this decline in metabolic rate could explain the low urinary concentrating ability of large mammals with long loops of Henle. Mitochondrial ultrastructural parameters were measured in the medullary thick ascending limbs (mTALs) of a series of nine mammalian genera ranging in body mass from 0.011 kg (bats) to approximately 400 kg (horses). The volume of mitochondria as a percent of mTAL cellular volume declined with increasing body mass (Mb-0.056). Inner mitochondrial membrane area per volume of mitochondrion also declined with increasing body mass (Mb-0.034), as did basolateral membrane area per unit mTAL cellular volume (Mb-0.075). Thus, not only do mitochondria occupy more volume of mTAL cells of smaller mammals, but those mitochondria are also more densely packed with cristae. Inner mitochondrial membrane area per unit volume of mTAL cell cytoplasm scaled as Mb-0.092. The decline in inner mitochondrial membrane area and basolateral membrane area per volume of mTAL cell may explain at least in part the relationship between body mass and renal concentrating ability in mammals of different sizes.


1995 ◽  
Vol 198 (3) ◽  
pp. 739-746 ◽  
Author(s):  
K E Conley ◽  
K A Christian ◽  
H Hoppeler ◽  
E R Weibel

The heart mitochondrial properties and the aerobic capacity (VO2max) of the rat (Sprague-Dawley breed) and the Cuban iguana (Cyclura nubila) were used to evaluate the relationship between the oxidative capacity of the heart and the maximum oxygen delivery rate. Both species are active at body temperatures of 37-39 degrees C, have similar heart mitochondrial volumes [Vmt; 0.43 +/- 0.02 ml (S.E.M.) in the rat and 0.48 +/- 0.02 ml in the iguana] and differ less than twofold in VO2max (29.2 +/- 1.6 and 16.9 +/- 0.6 ml min-1, respectively). We found that Vmt was closely correlated with VO2max in the rat (r2 = 0.77, P < 0.005) and the iguana (r2 = 0.82; P < 0.001). Furthermore, the inner mitochondrial membrane (cristae) area (Sim) per unit VO2max did not differ between the rat and the iguana (0.60 +/- 0.02 and 0.71 +/- 0.02 m2 min ml-1 O2, respectively). This correspondence of Sim/VO2max indicates that the rat and the iguana have the same cardiac oxidative capacity at the maximum oxygen delivery rate. These results suggest that, despite the differences between the cardiovascular systems of these species, the cardiac cost of delivering oxygen at the aerobic capacity is similar in this mammal and this reptile.


2007 ◽  
Vol 34 (S 2) ◽  
Author(s):  
D Siemen ◽  
Y Cheng ◽  
X Gu ◽  
P Bednarczyk ◽  
GG Haddad ◽  
...  

1999 ◽  
Vol 5 (S2) ◽  
pp. 1118-1119
Author(s):  
Heide Schatten ◽  
Marian Lewis

Spaceflight induced mitochondrial alterations have been reported for muscle and may be associated with altered physiological functions in space. Mitochondrial alterations are also indicative of preapoptotic events which are seen in greater amounts in cells exposed to spaceflight when compared with cells cultured at 1 g. Preapoptotic mitochondrial changes include alterations of processes at the inner mitochondrial membrane and can result in changes in mitochondrial volume. Higher amounts of oxidative stress during space flight may be one of the causes for changes which lead to apoptosis. Jurkat cells flown on the STS-76 space shuttle mission showed an increase in the number of cells with apoptotic bodies early in the mission and a time-dependent, microgravity-related increase in the Fas/APO-1 cell death factor. Here we investigated the morphology of mitochondria in Jurkat cells exposed to spaceflight during the STS-76 mission.


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