pH Homeostasis in Terrestrial Vertebrates: A Comparison of Traditional and New Concepts

Pörtner, Hans‐Otto

doi:10.1007/978-3-642-52363-2_3

Cited by 3 publications

(2 citation statements)

References 15 publications

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“…A further drop of O/N ratios to values around 3.0 indicated a change in the mixture of metabolized amino acids to preferred oxidative decarboxylation and catabolism of dicarboxylic, low O/N amino acids like asparagine, glutamic acid or glutamine. The benefit of this shift is an enhanced net-production of bicarbonate (Pörtner, 1995) supporting the compensation of pHi under acidic conditions. Elevated intracellular bicarbonate concentrations might also activate soluble adenylyl cyclases (sAC) as in different mammalian tissues (Chen et al, 2000).…”

Section: Discussionmentioning

confidence: 80%

Effects of environmental hypercapnia on animal physiology: A 13C NMR study of protein synthesis rates in the marine invertebrate Sipunculus nudus

Langenbuch

Bock

Leibfritz

et al. 2006

Comparative Biochemistry and Physiology Part A: Molecular &

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Global climate change is associated with a progressive rise in ocean CO 2 concentrations (hypercapnia) and, consequently, a drop in seawater pH. However, a comprehensive picture of the physiological mechanisms affected by chronic CO 2 stress in marine biota is still lacking. Here we present an analysis of protein biosynthesis rates in isolated muscle of the marine invertebrate Sipunculus nudus, a sediment dwelling worm living at various water depths. We followed the incorporation of 13 C-labelled phenylalanine into muscular protein via high-resolution NMR spectroscopy. Protein synthesis decreased by about 60% at a medium pH of 6.70 and a consequently lowered intracellular pH (pHi). The decrease in protein synthesis rates is much stronger than the concomitant suppression of protein degradation (60% versus 10-15%) possibly posing a threat to the cellular homeostasis of structural as well as functional proteins. Considering the progressive rise in ocean CO 2 concentrations, permanent disturbances of cellular protein turnover might seriously affect growth and reproductive performance in many marine organisms with as yet unexplored impacts on species density and composition in marine ecosystems.

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Section: Discussionmentioning

confidence: 80%

Effects of environmental hypercapnia on animal physiology: A 13C NMR study of protein synthesis rates in the marine invertebrate Sipunculus nudus

Langenbuch

Bock

Leibfritz

et al. 2006

Comparative Biochemistry and Physiology Part A: Molecular &

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“…Nonetheless, net H +equivalent ion exchange, which is equivalent to a net release of base under normocapnic control conditions, shifts to a reduced rate of base release during hypercapnia. Thereby, it reflects an increased net production of protons in metabolism, as expected from the proton balance of overall amino acid catabolism, which leads to ammonium formation in excess of bicarbonate formation and, consequently, net acid excretion (see Pörtner, 1989Pörtner, , 1995.…”

Section: Acid-base Regulationmentioning

confidence: 99%

Acid–Base Regulation, Metabolism and Energetics in Sipunculus Nudus As a Function of Ambient Carbon Dioxide Level

Pörtner

Reipschläger²,

Heisler³

1998

Journal of Experimental Biology

125

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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.

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Metabolic costs induced by lactate in the toadBufo marinus: new mechanism behind oxygen debt?

Pinz

Pörtner

2003

Journal of Applied Physiology

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Pinz, Ilka, and Hans-O. Pö rtner. Metabolic costs induced by lactate in the toad Bufo marinus: new mechanism behind oxygen debt?. J Appl Physiol 94: 1177 -1185 , 2003 . FirstpublishedNovember8,200210.1152/japplphysiol.00131. 2002The mechanism of an increase in metabolic rate induced by lactate was investigated in the toad Bufo marinus. Oxygen consumption (V O2) was analyzed in fully aerobic animals under hypoxic conditions (7% O 2 in air), accompanied by measurements of catecholamines in the plasma, and was measured in isolated hepatocytes in vitro under normoxia by using specific inhibitors of lactate proton symport [␣-cyano-4-hydroxycinnamate (CHC)] and sodium proton exchange (EIPA). The rise in metabolic rate in vivo can be elicited by infusions of hyperosmotic (previous findings) or isosmotic sodium lactate solutions (this study). Despite previous findings of reduced metabolic stimulation under the effect of adrenergic blockers, the increase in V O2 in vivo was not associated with elevated plasma catecholamine levels, suggesting local release and effect. In addition to the possible in vivo effect via catecholamines, lactate induced a rise in V O2 of isolated hepatocytes, depending on the concentration present in a weakly buffered Ringer solution at pH 7.0. No increase was found at higher pH values (7.4 or 7.8) or in HEPES-buffered Ringer solution. Inhibition of the Lac Ϫ -H ϩ transporter with ␣-CHC or of the Na ϩ /H ϩ exchanger with EIPA prevented the increase in metabolic rate. We conclude that increased V O2 at an elevated systemic lactate level may involve catecholamine action, but it is also caused by an increased energy demand of cellular acid-base regulation via stimulation of Na ϩ /H ϩ exchange and thereby Na ϩ -K ϩ -ATPase. The effect depends on entry of lactic acid into the cells via lactate proton symport, which is likely favored by low cellular surface pH. We suggest that these energetic costs should also be considered in other physiological phenomena, e.g., when lactate is present during excess, postexercise V O2.energy cost of acid-base regulation; excess postexercise oxygen consumption; hypoxia; lactate proton symport; oxygen consumption; sodium proton exchange IT IS WELL KNOWN THAT METABOLIC RATE remains elevated after anaerobic exercise, indicating a partial repayment of an oxygen debt [also called excess postexercise oxygen consumption (EPOC)] (6, 11). More recently, it has been found that the metabolic rate can rise with the onset of hypoxia, accompanied by an accumulation of lactate in the body fluids below a critical PO 2 (P c ) (30, 31). The rise in oxygen consumption below the P c was not only seen in an amphibian, Bufo marinus (31), but also in goldfish and rainbow trout (3). In all of these cases, the glycolytic end product lactate is present; however, the mechanisms causing the metabolic increment remain incompletely understood (e.g., Ref. 34).Pörtner et al. (34) demonstrated a cause-and-effect relationship between lactate accumulation and the rise in oxygen consumption in B. marin...

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pH Homeostasis in Terrestrial Vertebrates: A Comparison of Traditional and New Concepts

Cited by 3 publications

References 15 publications

Effects of environmental hypercapnia on animal physiology: A 13C NMR study of protein synthesis rates in the marine invertebrate Sipunculus nudus

Effects of environmental hypercapnia on animal physiology: A 13C NMR study of protein synthesis rates in the marine invertebrate Sipunculus nudus

Acid–Base Regulation, Metabolism and Energetics in Sipunculus Nudus As a Function of Ambient Carbon Dioxide Level

Metabolic costs induced by lactate in the toadBufo marinus: new mechanism behind oxygen debt?

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