Responses to Hypersaline Exposure in the Euryhaline Crayfish Pacifastacus Leniusculus: I. The Interaction between Ionic and Acid-base Regulation

1982 ◽  
Vol 99 (1) ◽  
pp. 425-445
Author(s):  
MICHÈLE G. WHEATLY ◽  
B. R. MCMAHON
Keyword(s):  
Carbonic Acid ◽  
Sea Water ◽  
Inorganic Ions ◽  
Pacifastacus Leniusculus ◽  
Acid Base Balance ◽  
Acid Base ◽  
Salinity Acclimation ◽  
Base Balance ◽  
Hypocapnic Alkalosis

Haemolymph iono- and osmoregulation and acid-base balance were recorded after 48 h exposure at 15 °C to a range of increasing ambient salinities (0, 25, 50 and 75% sea water) in the euryhaline crayfish Pacifastacus leniusculus (Dana). Except for K+, concentrations of all measured inorganic ions and osmolality were significantly elevated in 50 and 75% SW. When compared with ambient changes there was evidence of a transition from hyperto hypoionic regulation above 44% SW. Ca2+ was regulated for a constant blood-medium difference. A progressive reduction in total CO2 was recorded; pH was maintained except in 75% SW where a haemolymph acidosis developed. To permit calculation of CO2 tension (PCOCO2), carbon dioxide solubility coefficient (αCO2) and the apparent first dissociation constant of carbonic acid (p K'1) were experimentally determined in vitro. αCO2 decreased progressively with acclimation salinity but was unaffected by circulating protein. pK'1 decreased as a function both of physiological pH and increasing haemolymph ionic strength. PCOCO2 calculated using these empirical constants, progressively decreased with high-salinity acclimation. The resulting ‘hypocapnic alkalosis’ was partially offset by a metabolic acidosis, whose correlation with extracellular anisosmotic and intracellular isosmotic regulation is discussed.

Regulation of urea synthesis by acid-base balance in vivo: role of NH3 concentration

1987 ◽  
Vol 252 (2) ◽  
pp. F221-F225 ◽  
Author(s):  
S. Cheema-Dhadli ◽  
R. L. Jungas ◽  
M. L. Halperin
Keyword(s):  
Ammonium Concentration ◽  
Urea Synthesis ◽  
Carbamoyl Phosphate ◽  
Acid Base Balance ◽  
Acid Base ◽  
Fixed Rate ◽  
Rate Limiting Step ◽  
Base Balance

The purpose of this study was to clarify how changes in acid-base balance influence the rate of urea synthesis in vivo. Since ureagenesis was increased by an ammonium infusion into rats, regulation seemed to be a function of the blood ammonium concentration. The rate of urea synthesis was constant at a fixed rate of ammonium infusion and independent of the conjugate base infused, chloride or bicarbonate. The steady-state blood ammonium concentration was higher in the rats that developed metabolic acidosis. Thus it appeared that regulation was not directly mediated by this ammonium concentration per se. The rate of urea synthesis was also independent of the blood pH. Accordingly, the rate of urea synthesis was examined as a function of the plasma NH3 concentration. The rate of ureagenesis was found to be directly proportional to the plasma NH3 concentration. Assuming that plasma NH3 levels reflect those in mitochondria, the NH3 concentration yielding half-maximal rates of urea synthesis (close to 2 microM) was in the same range as Km for the rate-limiting step in ureagenesis, carbamoyl phosphate synthetase (EC 6.3.4.16). These results suggest that, at a constant ammonium concentration, the decreased rate of ureagenesis caused by a pH fall in vitro could reflect an acidosis-induced decline in the concentration of true substrate (NH3) for this pathway.

An Approach to the Problems of Acid-Base Balance

1970 ◽  
Vol 39 (2) ◽  
pp. 169-182 ◽  
Author(s):  
C. T. Kappagoda ◽  
R. J. Linden ◽  
H. M. Snow
Keyword(s):  
Sodium Bicarbonate ◽  
Respiratory Acidosis ◽  
Acid Base Balance ◽  
Acid Base ◽  
Titration Curves ◽  
Base Parameters ◽  
Base Balance ◽  
Acid Base Disturbance ◽  
Direct Extrapolation

1. The existing methods for assessing states of acidosis are discussed with particular reference to non-respiratory acidosis. Most of these methods are based either on the Henderson—Hasselbalch equation or on the direct extrapolation of in vitro studies on blood to the whole animal. The evidence available shows that these methods cannot be used to obtain an accurate assessment of disturbances of acid-base balance in the whole animal. 2. The experiments were designed to investigate the acid-base parameters of an animal when a respiratory acidosis was superimposed on a non-respiratory acidosis caused by the infusion of n HCl; from these experiments it was possible to construct CO2 titration curves at various levels of non-respiratory acidosis. 3. A scheme which is based upon the CO2 titration curves, has been proposed for assessing an acute acid-base disturbance in terms of its respiratory and non-respiratory components. 4. The use of sodium bicarbonate to correct a non-respiratory acidosis was investigated, and it was shown that the amount of sodium bicarbonate required varied with the rate of infusion. No firm predictions could be made regarding the dose of bicarbonate required, but from the results of the present experiments an infusion rate of 0·1 mEq kg−1 min−1 is recommended in dogs.

scholarly journals pH-dependent regulation of the α-subunit of H+-K+-ATPase (HKα2)

2011 ◽  
Vol 301 (3) ◽  
pp. F536-F543 ◽  
Author(s):  
Juan Codina ◽  
Timothy S. Opyd ◽  
Zachary B. Powell ◽  
Cristina M. Furdui ◽  
Snezana Petrovic ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Immunoblot Analysis ◽  
Acid Base Balance ◽  
Acid Base ◽  
Membrane Expression ◽  
Α Subunit ◽  
Hek 293 ◽  
Genetic Ablation ◽  
Base Balance

The H+-K+-ATPase α-subunit (HKα2) participates importantly in systemic acid-base homeostasis and defends against metabolic acidosis. We have previously shown that HKα2 plasma membrane expression is regulated by PKA (Codina J, Liu J, Bleyer AJ, Penn RB, DuBose TD Jr. J Am Soc Nephrol 17: 1833–1840, 2006) and in a separate study demonstrated that genetic ablation of the proton-sensing Gs-coupled receptor GPR4 results in spontaneous metabolic acidosis (Sun X, Yang LV, Tiegs BC, Arend LJ, McGraw DW, Penn RB, Petrovic S. J Am Soc Nephrol 21: 1745–1755, 2010). In the present study, we investigated the ability of chronic acidosis and GPR4 to regulate HKα2 expression in HEK-293 cells. Chronic acidosis was modeled in vitro by using multiple methods: reducing media pH by adjusting bicarbonate concentration, adding HCl, or by increasing the ambient concentration of CO2. PKA activity and HKα2 protein were monitored by immunoblot analysis, and HKα2 mRNA, by real-time PCR. Chronic acidosis did not alter the expression of HKα2 mRNA; however, PKA activity and HKα2 protein abundance increased when media pH decreased from 7.4 to 6.8. Furthermore, this increase was independent of the method used to create chronic acidosis. Heterologous expression of GPR4 was sufficient to increase both basal and acid-stimulated PKA activity and similarly increase basal and acid-stimulated HKα2 expression. Collectively, these results suggest that chronic acidosis and GPR4 increase HKα2 protein by increasing PKA activity without altering HKα2 mRNA abundance, implicating a regulatory role of pH-activated GPR4 in homeostatic regulation of HKα2 and acid-base balance.

scholarly journals Metabolic component of intestinal Pco 2during dysoxia

2000 ◽  
Vol 89 (6) ◽  
pp. 2422-2429 ◽  
Author(s):  
Ovais Raza ◽  
Robert Schlichtig
Keyword(s):  
Blood Flow ◽  
Carbonic Acid ◽  
Respiratory Acidosis ◽  
Tissue Fluid ◽  
Acid Base Balance ◽  
Acid Base ◽  
First Order Kinetics ◽  
Base Balance ◽  
Buffer Base ◽  
Made In

The adequacy of intestinal perfusion during shock and resuscitation might be estimated from intestinal tissue acid-base balance. We examined this idea from the perspective of conventional blood acid-base physicochemistry. As the O2 supply diminishes with failing blood flow, tissue acid-base changes are first “respiratory,” with CO2 coming from combustion of fuel and stagnating in the decreasing blood flow. When the O2supply decreases to critical, the changes become “metabolic” due to lactic acid. In blood, the respiratory vs. metabolic distinction is conventionally made using the buffer base principle, in which buffer base is the sum of HCO3 − and noncarbonate buffer anion (A−). During purely respiratory acidosis, buffer base stays constant because HCO3 − cannot buffer its own progenitor, carbonic acid, so that the rise of HCO3 − equals the fall of A−. During anaerobic “metabolism,” however, lactate's H+ is buffered by both A− and HCO3 −, causing buffer base to decrease. We quantified the partitioning of lactate's H+ between HCO3 − and A−buffer in anoxic intestine by compressing intestinal segments of anesthetized swine into a steel pipe and measuring Pco 2 and lactate at 5- to 10-min intervals. Their rises followed first-order kinetics, yielding k = 0.031 min−1 and half time = ∼22 min. Pco 2 vs. lactate relations were linear. Over 3 h, lactate increased by 31 ± 3 mmol/l tissue fluid (mM) and Pco 2 by ∼17 mM, meaning that one-half of lactate's H+ was buffered by tissue HCO3 − and one-half by A−. The data were consistent with a lumped p K a value near 6.1 and total A− concentration of ∼30 mmol/kg. We conclude that the respiratory vs. metabolic distinction could be made in tissue by estimating tissue buffer base from measured pH and Pco 2.

Blood Acid-Base Balance in the Lugworm Arenicola Marina Ventilating in Hypo- or Hyperoxic Sea Water

1989 ◽  
Vol 142 (1) ◽  
pp. 143-153
Author(s):  
ANDRÉ TOULMOND ◽  
CATHERINE TCHERNIGOVTZEFF
Keyword(s):  
Time Course ◽  
Sea Water ◽  
Acid Base Balance ◽  
Acid Base ◽  
Arenicola Marina ◽  
Base Balance

The time course of variation in blood acid-base balance was examined in lugworms, Arenicola marina (L.), experimentally acclimated for up to 72 h in hypoxic (PO2 = 80 mmHg) (1 mmHg = 133.3 Pa), normoxic (PO2 = 160 mmHg) or hyperoxic (PO2 = 500 mmHg) sea water. In hyperoxic animals, a blood acidosis is entirely compensated 12 h after the beginning of the acclimation. In hypoxic animals, a blood alkalosis develops very quickly, persists and increases, reaching a maximum 72h after the beginning of the acclimation. In both cases, variation in blood acid-base balance is mainly of respiratory origin. These data are consistent with previous results showing that the lugworm hypoventilates in hyperoxic sea water and hyperventilates in hypoxic sea water.

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