scholarly journals Acid-base regulation, metabolism and energetics in sipunculus nudus as a function of ambient carbon dioxide level

1998 ◽  
Vol 201 (1) ◽  
pp. 43-55 ◽  
Author(s):  
H O Pörtner ◽  
A Reipschläger ◽  
N Heisler
Keyword(s):  
Ammonium Excretion ◽  
Ion Transfer ◽  
Energy Status ◽  
Intracellular Acidosis ◽  
Acid Base ◽  
Sipunculus Nudus ◽  
Acid Base Status ◽  
Net Release

Changes in the rates of oxygen consumption and ammonium excretion, in intra- and extracellular acid-base status and in the rate of H+-equivalent ion transfer between animals and ambient water were measured during environmental hypercapnia in the peanut worm Sipunculus nudus. During exposure to 1 % CO2 in air, intracellular and coelomic plasma PCO2 values rose to levels above those expected from the increase in ambient CO2 tension. Simultaneously, coelomic plasma PO2 was reduced below control values. The rise in PCO2 also induced a fall in intra- and extracellular pH, but intracellular pH was rapidly and completely restored. This was achieved during the early period of hypercapnia at the expense of a non-respiratory increase in the extracellular acidosis. The pH of the extracellular space was only partially compensated (by 37 %) during long-term hypercapnia. The net release of basic equivalents under control conditions turned to a net release of protons to the ambient water before a net, albeit reduced, rate of base release was re-established after a new steady state had been achieved with respect to acid-base parameters. Hypercapnia also affected the mode and rate of metabolism. It caused the rate of oxygen consumption to fall, whereas the rate of ammonium excretion remained constant or even increased, reflecting a reduction of the O/N ratio in both cases. The transient intracellular acidosis preceded a depletion of the phosphagen phospho-l-arginine, an accumulation of free ADP and a decrease in the level of Gibbs free energy change of ATP hydrolysis, before replenishment of phosphagen and restoration of pHi and energy status occurred in parallel. In conclusion, long-term hypercapnia in vivo causes metabolic depression, a parallel shift in acid-base status and increased gas partial pressure gradients, which are related to a reduction in ventilatory activity. The steady-state rise in H+-equivalent ion transfer to the environment reflects an increased rate of production of protons by metabolism. This observation and the reduction of the O/N ratio suggest that a shift to protein/amino acid catabolism has taken place. Metabolic depression prevails, with completely compensated intracellular acidosis during long-term hypercapnia eliminating intracellular pH as a significant factor in the regulation of metabolic rate in vivo. Fluctuating levels of the phosphagen, of free ADP and in the ATP free energy change values independent of pH are interpreted as being correlated with oscillating ATP turnover rates during early hypercapnia and as reflecting a tight coupling of ATP turnover and energy status via the level of free ADP.

scholarly journals Damage to the gastric epithelium activates cellular bicarbonate secretion via SLC26A9 Cl−/HCO3−exchange

2010 ◽  
Vol 299 (1) ◽  
pp. G255-G264 ◽  
Author(s):  
Elise S. Demitrack ◽  
Manoocher Soleimani ◽  
Marshall H. Montrose
Keyword(s):  
Interstitial Fluid ◽  
Gastric Epithelium ◽  
Acid Base ◽  
Surface Ph ◽  
Two Photon ◽  
Acid Base Status ◽  
Genetic Deletion ◽  
Knockout Animals ◽  
Tissue Compartments

Gastric surface pH (pHo) transiently increases in response to focal epithelial damage. The sources of that increase, either from paracellular leakage of interstitial fluid or transcellular acid/base fluxes, have not been determined. Using in vivo microscopy approaches we measured pHowith Cl-NERF, tissue permeability with intravenous fluorescent-dextrans to label interstitial fluid (paracellular leakage), and gastric epithelial intracellular pH (pHi) with SNARF-5F (cellular acid/base fluxes). In response to two-photon photodamage, we found that cell-impermeant dyes entered damaged cells from luminal or tissue compartments, suggesting a possible slow transcellular, but not paracellular, route for increased permeability after damage. Regarding cytosolic acid/base status, we found that damaged cells acidified (6.63 ± 0.03) after photodamage, compared with healthy surface cells both near (7.12 ± 0.06) and far (7.07 ± 0.04) from damage ( P < 0.05). This damaged cell acidification was further attenuated with 20 μM intravenous EIPA (6.34 ± 0.05, P < 0.05) but unchanged by addition of 0.5 mM luminal H2DIDS (6.64 ± 0.08, P > 0.05). Raising luminal pH did not realkalinize damaged cells, suggesting that the mechanism of acidification is not attributable to leakiness to luminal protons. Inhibition of apical HCO3−secretion with 0.5 mM luminal H2DIDS or genetic deletion of the solute-like carrier 26A9 (SLC26A9) Cl−/HCO3−exchanger blocked the pHoincrease normally observed in control animals but did not compromise repair of damaged tissue. Addition of exogenous PGE2significantly increased pHoin wild-type, but not SLC26A9 knockout, animals, suggesting that prostaglandin-stimulated HCO3−secretion is fully mediated by SLC26A9. We conclude that cellular HCO3−secretion, likely through SLC26A9, is the dominant mechanism whereby surface pH transiently increases in response to photodamage.

Role of ion transfer processes in acid-base regulation with temperature changes in fish

1984 ◽  
Vol 246 (4) ◽  
pp. R441-R451 ◽  
Author(s):  
N. Heisler
Keyword(s):  
Ion Transfer ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Fish Tissues ◽  
Model Calculations ◽  
Temperature Changes ◽  
Transfer Processes ◽  
Transfer Mechanisms

The contributions of transmembrane and transepithelial ion transfer processes and of nonbicarbonate buffering to the in vivo acid-base regulation have been evaluated. Model calculations were performed utilizing experimental data on transepithelial transfer of ions relevant for the acid-base regulation, the intracellular buffering properties of fish tissues, and the behavior of intracellular and extracellular pH and bicarbonate concentration with changes of temperature. The results of these studies indicate that the changes in the pK values of physiological nonbicarbonate buffers with changes in temperature support the adjustment of pH to lower values with rising temperature; however, transmembrane and transepithelial ion transfer mechanisms determine the acid-base regulation of intracellular and extracellular compartments.

Metabolic and energy correlates of intracellular pH in progressive fatigue of squid (L. brevis) mantle muscle

1996 ◽  
Vol 271 (5) ◽  
pp. R1403-R1414 ◽  
Author(s):  
H. O. Portner ◽  
E. Finke ◽  
P. G. Lee
Keyword(s):  
Free Energy ◽  
Critical Velocity ◽  
Energy Levels ◽  
High Energy ◽  
Swimming Velocity ◽  
High Energy Phosphates ◽  
Energy Status ◽  
Intracellular Acidosis ◽  
Model Calculations

Squid (Lolliguncula brevis) were exercised at increasing swimming speeds to allow us to analyze the correlated changes in intracellular metabolic, acid-base, and energy status of the mantle musculature. Beyond a critical swimming velocity of 1.5 mantle lengths/s, an intracellular acidosis developed that was caused by an initial base loss from the cells, the onset of respiratory acidification, and, predominantly, octopine formation. The acidosis was correlated with decreasing levels of phospho-L-arginine and, thus, supported ATP buffering at the expense of the phosphagen. Monohydrogenphosphate, the actual substrate of glycogen phosphorylase accumulated, enabling glycogen degradation, despite progressive acidosis. In addition to octopine, succinate, and glycerophosphate accumulation, the onset of acidosis characterizes the critical velocity and indicates the transition to a non-steady-state time-limited situation. Accordingly, swimming above the critical velocity caused cellular energy levels (in vivo Gibbs free energy change of ATP hydrolysis) to fall. A minimal value was reached at about -45 kJ/mol. Model calculations demonstrate that changes in free Mg2+ levels only minimally affect ATP free energy, but minimum levels are relevant in maintaining functional concentrations of Mg(2+)-complexed adenylates. Model calculations also reveal that phosphagen breakdown enabled L. brevis to reach swimming speeds about three times higher than the critical velocity. Comparison of two offshore squid species (Loligo pealei and Illex illecebrosus) with the estuarine squid L.brevis indicates that the latter uses a strategy to delay the exploitation of high-energy phosphates and protect energy levels at higher than the minimum levels (-42 kJ/mol) characterizing fatigue in the other species. A more economical use of anaerobic resources and an early reduction in performance may enable L. brevis to tolerate more extreme environmental conditions in shallow estuarine waters and even hypoxic environments and to prevent a fatal depletion of energy stores.

scholarly journals Modulation of the cost of pHi regulation during metabolic depression: a (31)P-NMR study in invertebrate (Sipunculus nudus) isolated muscle

2000 ◽  
Vol 203 (16) ◽  
pp. 2417-2428 ◽  
Author(s):  
H.O. Portner ◽  
C. Bock ◽  
A. Reipschlager
Keyword(s):  
Steady State ◽  
Marine Invertebrate ◽  
Metabolic Depression ◽  
Acid Base ◽  
Extracellular Acidosis ◽  
Nmr Study ◽  
Sipunculus Nudus ◽  
Delayed Recovery ◽  
Dimethyl Amiloride

Extracellular acidosis has been demonstrated to play a key role in the process of metabolic depression under long-term environmental stress, exemplified in the marine invertebrate Sipunculus nudus. These findings led to the hypothesis that acid-base regulation is associated with a visible cost depending on the rate and mode of H(+)-equivalent ion exchange. To test this hypothesis, the effects of different ion-transport inhibitors on the rate of pH recovery during hypercapnia, on energy turnover and on steady-state acid-base variables were studied in isolated body wall musculature of the marine worm Sipunculus nudus under control conditions (pHe 7.90) and during steady-state extracellular acidosis (pHe 7.50 or 7.20) by in vivo (31)P-NMR and oxygen consumption analyses. During acute hypercapnia (2 % CO(2)), recovery of pHi was delayed at pHe 7.5 compared with pHe 7.9. Inhibition of the Na(+)/H(+)-exchanger by 5-(N,N-dimethyl)-amiloride (DMA) at pHe 7.5 delayed recovery even further. This effect was much smaller at pHe 7.9. Inhibition of anion exchange by the addition of the transport inhibitor 4, 4′-diisothiocyanatostilbene-2,2′-disulphonic acid (DIDS) prevented pH recovery at pHe 7.5 and delayed recovery at pHe 7.9, in accordance with an effect on Na(+)-dependent Cl(−)/HCO(3)(−) exchange. The effects of ouabain, DIDS and DMA on metabolic rate were reduced at low pHe, thereby supporting the conclusion that acidosis caused the ATP demand of Na(+)/K(+)-ATPase to fall. This reduction occurred via an inhibiting effect on both Na(+)/H(+)- and Na(+)-dependent Cl(−)/HCO(3)(−) (i.e. Na(+)/H(+)/Cl(−)/HCO(3)(−)) exchange in accordance with a reduction in the ATP demand for acid-base regulation during metabolic depression. Considering the ATP stoichiometries of the two exchangers, metabolic depression may be supported by the predominant use of Na(+)/H(+)/Cl(−)/HCO(3)(−) exchange under conditions of extracellular acidosis.

The Effect of Long-Term Aerial Exposure on Heart Rate, Ventilation, Respiratory Gas Exchange and Acid-Base Status in the Crayfish Austropotamobius Pallipes

1981 ◽  
Vol 92 (1) ◽  
pp. 109-124
Author(s):  
E. W. TAYLOR ◽  
MICHÈLE G. WHEATLY
Keyword(s):  
Heart Rate ◽  
Lactic Acid ◽  
O2 Consumption ◽  
Aerial Exposure ◽  
Acid Base ◽  
Bicarbonate Buffer ◽  
Content Difference ◽  
Acid Base Status ◽  
Lactate Levels

1. When first removed into air, crayfish showed transient increases in heart rate (fH) and scaphognathite rate (fR) which rapidly recovered to submerged levels and were unchanged for 24 h. The rate of O2 consumption(Moo2) increased from an initially low level and was then maintained for 24 h in air at the same level as in settled submerged animals. 2. There was an initial acidosis in the haemolymph which was both respiratory and metabolic due to the accumulation of CO2 and lactate. Progressive compensation by elevation of the levels of bicarbonate buffer in the haemolymph and reduction of circulating lactate levels returned pH towards submerged levels after 24 h in air. 3. Exposure to air resulted in a marked internal hypoxia with haemolymph O2, tensions, both postbranchial Pa, oo2 and prebranchial Pv, oo2, remaining low throughout the period of exposure. The oxygen content or the haemolymph was initially reduced, with a - vOO2 content difference close to zero. Within 24 h both Ca, oo2 and Cv, OO2 had returned towards their levels in submerged animals. These changes are explained by the Bohr shift on the haemocyanin consequent upon the measured pH changes. 4. After 48 h in air, MO2 and fH were significantly reduced and ventilation became intermittent. There was a slight secondary acidosis, increase in lactic acid levels and reduction in a - vO2 content difference in the haemolymph. 5. When crayfish were returned to water after 24 h in air, MOO2, fHfR were initially elevated by disturbance and there was a period of hyperventilation. In the haemolymph there was an initial slight alkalosis, and an increase in Ca, OO2 lactic acid. All variables returned to their settled submerged levels within 8 h.

Loss of the NHE2 Na+/H+ exchanger has no apparent effect on diarrheal state of NHE3-deficient mice

2001 ◽  
Vol 281 (6) ◽  
pp. G1385-G1396 ◽  
Author(s):  
Clara Ledoussal ◽  
Alison L. Woo ◽  
Marian L. Miller ◽  
Gary E. Shull
Keyword(s):  
Absorptive Capacity ◽  
Apparent Effect ◽  
Acid Base ◽  
Intestinal Brush Border ◽  
Apparent Reduction ◽  
Acid Base Status ◽  
Deficient Mice ◽  
Additional Loss ◽  
Partial Compensation

The expression of NHE2 and NHE3 on intestinal-brush border membranes suggests that both Na+/H+ exchangers serve absorptive functions. Studies with knockout mice showed that the loss of NHE3, but not NHE2, causes diarrhea, demonstrating that NHE3 is the major absorptive exchanger and indicating that any remaining absorptive capacity contributed by NHE2 is not sufficient to compensate fully for the loss of NHE3. To test the hypothesis that NHE2 provides partial compensation for the diarrheal state of NHE3-deficient mice, we crossed doubly heterozygous mice carrying null mutations in the Nhe2and Nhe3 genes and analyzed the phenotypes of their offspring. The additional loss of NHE2 in NHE3-deficient mice caused no apparent reduction in viability, no further impairment of systemic acid-base status or increase in aldosterone levels, and no apparent worsening of the diarrheal state. These in vivo phenotypic correlates of the absorptive defect suggest that the NaCl, HCO[Formula: see text], and fluid absorption that is dependent on apical Na+/H+ exchange is due overwhelmingly to the activity of NHE3, with little contribution from NHE2.

Long-term Effects of Dietary Anion-Cation Balance on Acid-Base Status and Bone Morphology in Reproducing Ewes

2003 ◽  
Vol 50 (10) ◽  
pp. 488-495 ◽  
Author(s):  
L. Espino ◽  
F. Guerrero ◽  
M. L. Suarez ◽  
G. Santamarina ◽  
A. Goicoa ◽  
...  
Keyword(s):  
Long Term Effects ◽  
Bone Morphology ◽  
Acid Base ◽  
Acid Base Status

scholarly journals Metabolism and energetics in squid (Illex illecebrosus, Loligo pealei) during muscular fatigue and recovery

1993 ◽  
Vol 265 (1) ◽  
pp. R157-R165 ◽  
Author(s):  
H. O. Portner ◽  
D. M. Webber ◽  
R. K. O'Dor ◽  
R. G. Boutilier
Keyword(s):  
Energy Production ◽  
Detrimental Effect ◽  
Anaerobic Metabolism ◽  
Energy Status ◽  
Acid Base ◽  
Mantle Tissue ◽  
Anaerobic Energy ◽  
Acid Base Status ◽  
Postexercise Recovery ◽  
Loligo Pealei

The concentrations of intermediate and end products of anaerobic energy metabolism and of free amino acids were determined in mantle musculature and blood sampled from cannulated, unrestrained squid (Loligo pealei, Illex illecebrosus) under control conditions, after fatigue from increasing levels of exercise, and during postexercise recovery. Phosphagen depletion, accumulation of octopine (more so in Illex than in Loligo), and accumulation of succinate indicate that anaerobic metabolism contributes to energy production before fatigue. Proline was a substrate of metabolism in Loligo, as indicated by its depletion in the mantle. In both species, there was no evidence of catabolism of ATP beyond AMP. A comparison of the changes in the free and total levels of adenylates and the phosphagen indicates an earlier detrimental effect of fatigue on the energy status in Loligo. The acidosis provoked by octopine formation in Illex was demonstrated to promote the use of the phosphagen and to protect the free energy change of ATP such that the anaerobic scope of metabolism during swimming is extended and expressed more in Illex than in Loligo. In both species, there was no decrease in the sum of phospho-L-arginine, octopine, and L-arginine, and thus no release of octopine from the mantle, thereby supporting our earlier claim that octopine and associated protons are recycled in the mantle tissue. Overall, the metabolic strategy of Loligo is much less disturbing for the acid-base status. This strategy and the alternative strategy of Illex to keep acidifying protons in the tissue may be important for the protection of hemocyanin function in the two species.

Cellular actions of cAMP on HCO3(-)-secreting cells of rabbit CCD: dependence on in vivo acid-base status

1994 ◽  
Vol 266 (4) ◽  
pp. F528-F535 ◽  
Author(s):  
C. Emmons ◽  
J. B. Stokes
Keyword(s):  
Anion Exchanger ◽  
Collecting Duct ◽  
Basolateral Membrane ◽  
Disulfonic Acid ◽  
Intercalated Cells ◽  
Cortical Collecting Duct ◽  
Acid Base ◽  
Acid Base Status

HCO3- secretion by cortical collecting duct (CCD) occurs via beta-intercalated cells. In vitro CCD HCO3- secretion is modulated by both the in vivo acid-base status of the animal and by adenosine 3',5'-cyclic monophosphate (cAMP). To investigate the mechanism of cAMP-induced HCO3- secretion, we measured intracellular pH (pHi) of individual beta-intercalated cells of CCDs dissected from alkali-loaded rabbits perfused in vitro. beta-Intercalated cells were identified by demonstrating the presence of an apical anion exchanger (cell alkalinization in response to removal of lumen Cl-). After 180 min of perfusion to permit decrease of endogenous cAMP, acute addition of 0.1 mM 8-bromo-cAMP or 1 microM isoproterenol to the bath caused a transient cellular alkalinization (> 0.20 pH units). In the symmetrical absence of either Na+, HCO3-, or Cl-, cAMP produced no change in pHi. Basolateral dihydrogen 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (0.1 mM) for 15 min before cAMP addition also prevented this alkalinization. In contrast to the response of cells from alkali-loaded rabbits, addition of basolateral cAMP to CCDs dissected from normal rabbits resulted in an acidification of beta-intercalated cells (approximately 0.20 pH units). The present studies demonstrate the importance of the in vivo acid-base status of the animal in the regulation of CCD HCO3- secretion by beta-intercalated cells. The results identify the possible existence of a previously unrecognized Na(+)-dependent Cl-/HCO3- exchanger on the basolateral membrane of beta-intercalated cells in alkali-loaded rabbits.

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