Acid–Base Regulation and Ammonia Excretion in Cephalopods: An Ontogenetic Overview

2016 ◽  
pp. 275-298 ◽  
Author(s):  
Marian Hu ◽  
Yung-Che Tseng
Keyword(s):  
Ammonia Excretion ◽  
Acid Base

Acid-Base Effects of Combined Renal Deletion of NBCe1-A and NBCe1-B

2022 ◽  
Author(s):  
Hyun-Wook Lee ◽  
Jill W. Verlander ◽  
Gary E Shull ◽  
Autumn N. Harris ◽  
I. David Weiner
Keyword(s):  
Proximal Tubule ◽  
Splice Variant ◽  
Molecular Mechanisms ◽  
Ammonia Excretion ◽  
Basal Diet ◽  
Acid Base ◽  
Outer Medulla ◽  
Ammonia Metabolism ◽  
Induced Changes ◽  
Acid Loading

The molecular mechanisms regulating ammonia metabolism are fundamental to acid-base homeostasis. Deleting the A splice variant of the Na⁺-bicarbonate cotransporter, electrogenic, isoform 1 (NBCe1-A) partially blocks the effect of acidosis to increase urinary ammonia excretion, and this appears to involve the dysregulated expression of ammoniagenic enzymes in the proximal tubule (PT) in the cortex, but not in the outer medulla (OM). A second NBCe1 splice variant, NBCe1-B, is present throughout the PT, including the OM, where NBCe1-A is not present. The current studies determined the effects of combined renal deletion of NBCe1-A and NBCe1-B on systemic and proximal tubule ammonia metabolism. We generated NBCe1-A/B deletion using Cre-loxP techniques and used Cre-negative mice as controls. Since renal NBCe1-A and NBCe1-B expression is limited to the proximal tubule, Cre-positive mice had proximal tubule NBCe1-A/B deletion (PT-NBCe1-A/B KO). While on basal diet, PT-NBCe1-A/B KO mice had severe metabolic acidosis, yet urinary ammonia excretion was not changed significantly. PT-NBCe1-A/B KO decreased expression of phosphate-dependent glutaminase (PDG) and phospho­enol­pyruvate carboxy­kinase (PEPCK) and increased expression of glutamine synthetase (GS), an ammonia recycling enzyme, in PT in both the cortex and OM. Exogenous acid-loading increased ammonia excretion in control mice, but PT-NBCe1-A/B KO prevented any increase. PT-NBCe1-A/B KO significantly blunted acid loading-induced changes in PDG, PEPCK, and GS expression in the proximal tubule in both the cortex and OM. We conclude that NBCe1-B, at least in the presence of NBCe1-A deletion, contributes to proximal tubule ammonia metabolism in the OM and thereby to systemic acid-base regulation.

Changes in metabolic rate and N excretion in the marine invertebrateSipunculus nudusunder conditions of environmental hypercapnia

2002 ◽  
Vol 205 (8) ◽  
pp. 1153-1160 ◽  
Author(s):  
M. Langenbuch ◽  
H. O. Pörtner
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Metabolic Rate ◽  
Intracellular Ph ◽  
Energy Demand ◽  
Control Level ◽  
Ammonia Excretion ◽  
Amino Acid Catabolism ◽  
Acid Base ◽  
Selection Of

SUMMARYIncreased CO2 partial pressures (hypercapnia) as well as hypoxia are natural features of marine environments like the intertidal zone. Nevertheless little is known about the specific effects of CO2 on metabolism, except for the well-described effects on acid—base variables and regulation. Accordingly, the sediment-dwelling worm Sipunculus nudus was used as an experimental model to investigate the correlation of acid—base-induced metabolic depression and protein/amino acid catabolism, by determining the rates of oxygen consumption, ammonia excretion and O/N ratios in non-perfused preparations of body wall musculature at various levels of extra- and intracellular pH, PCO2 and [HCO3-]. A decrease in extracellular pH from control level (7.9) to 6.7 caused a reduction in aerobic metabolic rate of both normocapnic and hypercapnic tissues by 40-45 %. O/N ratios of 4.0-4.5 under control conditions indicate that amino acid catabolism meets the largest fraction of aerobic energy demand. A significant 10-15 % drop in ammonia excretion, a simultaneous reduction of O/N ratios and a transient accumulation of intracellular bicarbonate during transition to extreme acidosis suggest a reduction in net amino acid catabolism and a shift in the selection of amino acids used,favouring monoamino dicarboxylic acids and their amines (asparagine,glutamine, aspartic and glutamic acids). A drop in intracellular pH was identified as mediating this effect. In conclusion, the present data provide evidence for a regulatory role of intracellular pH in the selection of amino acids used by catabolism.

Nitrogen excretion in germ-free and conventional chickens: effects of an alkali load

1978 ◽  
Vol 39 (1) ◽  
pp. 99-104 ◽  
Author(s):  
J. Okumura ◽  
D. Hewitt ◽  
Marie E. Coates
Keyword(s):  
Amino Acids ◽  
Uric Acid ◽  
Ammonia Excretion ◽  
Nitrogen Excretion ◽  
Acid Base Balance ◽  
Acid Base ◽  
Total N ◽  
Germ Free ◽  
Base Balance ◽  
Micro Organisms

1. Groups of three colostomized germ-free (GF) and conventional (CV) chickens aged 4 months were maintained for successive periods of 8 d on a diet containing 200 g casein/kg without and with sodium bicarbonate at the rate of 20 mmol/d and a nitrogen-free diet without and with NaHCO3at 9 mmol/d. Urine and faeces were collected during the last 3 d of each period.2. Total N, uric acid- and ammonia-N were determined in urine and total N in faeces. Amino acids were measured in hydrolysates of faeces collected during the periods when no NaHCO3was included in the diets.3. The CV birds excreted more N on the casein diets but less on the N-free diets than did their GF counterparts, the differences being mainly shown in the urine.4. On both diets hydrolysates of the faeces of CV birds contained smaller amounts of amino acids. On the N-free diet the proportions (g/160 g N) of serine, proline and threonine were reduced, suggesting some conservation of endogenous N by micro-organisms, and the proportions of histidine, alanine, lysine and methionine increased, possibly through microbial synthesis; on the casein diet, proportions of most amino acids were less, probably because bacterial deamination had occurred.5. Urinary excretion of total N, uric acid and ammonia was much greater on the casein than on the N-free diets. Inclusion of NaHCO3caused a sharp fall in urinary ammonia on both diets and in both environments.6. It was concluded that the level of dietary protein and the regulation of acid-base balance have more effect than microbial activity on the urinary ammonia excretion.

scholarly journals Effect of hypokalemia on renal expression of the ammonia transporter family members, Rh B Glycoprotein and Rh C Glycoprotein, in the rat kidney

2011 ◽  
Vol 301 (4) ◽  
pp. F823-F832 ◽  
Author(s):  
Ki-Hwan Han ◽  
Hyun-Wook Lee ◽  
Mary E. Handlogten ◽  
Jesse M. Bishop ◽  
Moshe Levi ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Metabolic Alkalosis ◽  
Collecting Duct ◽  
Family Members ◽  
Ammonia Excretion ◽  
Intercalated Cells ◽  
Acid Base ◽  
Ammonia Metabolism ◽  
Transporter Family ◽  
Base Disorder

Hypokalemia is a common electrolyte disorder that increases renal ammonia metabolism and can cause the development of an acid-base disorder, metabolic alkalosis. The ammonia transporter family members, Rh B glycoprotein (Rhbg) and Rh C glycoprotein (Rhcg), are expressed in the distal nephron and collecting duct and mediate critical roles in acid-base homeostasis by facilitating ammonia secretion. In the current studies, the effect of hypokalemia on renal Rhbg and Rhcg expression was examined. Normal Sprague-Dawley rats received either K+-free or control diets for 2 wk. Rats receiving the K+-deficient diet developed hypokalemia and metabolic alkalosis associated with significant increases in both urinary ammonia excretion and urine pH. Rhcg expression increased in the outer medullary collecting duct (OMCD). In OMCD intercalated cells, hypokalemia resulted in more discrete apical Rhcg expression and a marked increase in apical plasma membrane immunolabel. In principal cells, in the OMCD, hypokalemia increased both apical and basolateral Rhcg immunolabel intensity. Cortical Rhcg expression was not detectably altered by immunohistochemistry, although there was a slight decrease in total expression by immunoblot analysis. Rhbg protein expression was decreased slightly in the cortex and not detectably altered in the outer medulla. We conclude that in rat OMCD, hypokalemia increases Rhcg expression, causes more polarized apical expression in intercalated cells, and increases both apical and basolateral expression in the principal cell. Increased plasma membrane Rhcg expression in response to hypokalemia in the rat, particularly in the OMCD, likely contributes to the increased ammonia excretion and thereby to the development of metabolic alkalosis.

Renal regulation of acid-base balance in the bullfrog

1961 ◽  
Vol 201 (6) ◽  
pp. 980-986 ◽  
Author(s):  
Hisato Yoshimura ◽  
Masateru Yata ◽  
Minoru Yuasa ◽  
Robert A. Wolbach
Keyword(s):  
Carbonic Anhydrase ◽  
Ammonia Excretion ◽  
Respiratory Acidosis ◽  
Acid Base Balance ◽  
Acid Base ◽  
Urinary Ph ◽  
Base Balance ◽  
Chloride Excretion ◽  
Acid Load ◽  
Renal Carbonic Anhydrase

Renal mechanisms for the maintenance of acid-base balance were studied in the normal bullfrog, during metabolic and respiratory acidosis, and after carbonic anhydrase inhibition. Following intravenous administration of 0.3–12 mmole HCl/ kg, as 0.1 n HCl, urinary pH (initially pH 6.3–7.7) did not change significantly. However, urinary ammonia excretion increased more than twofold, and within 3–5 days the cumulative increase was equivalent to the acid load given. Despite the increased ammonia excretion, chloride excretion did not increase after acid loading. In both normal and acidotic bullfrogs ammonia excretion was correlated with an increase in urinary pH. Respiratory acidosis in the small frog, Rana limnocharis, produced by exposure to 6.4% CO2 in air, induced neither urinary acidification nor increased ammonia excretion; both urinary sodium and bicarbonate excretion increased. When renal carbonic anhydrase was inhibited by acetazoleamide injection, urine flow, sodium excretion, and bicarbonate excretion increased markedly, urinary pH increased slightly, and urinary ammonia excretion remained unchanged. These renal responses to acidosis are compared with those of the acidotic dog.

Sodium–hydrogen exchangers in the nematode Caenorhabditis elegans: investigations towards their potential role in hypodermal H+ excretion, Na+ uptake, and ammonia excretion, as well as acid–base balance

2017 ◽  
Vol 95 (9) ◽  
pp. 623-632 ◽  
Author(s):  
Aida Adlimoghaddam ◽  
Michael J. O’Donnell ◽  
Alex Quijada-Rodriguez ◽  
Dirk Weihrauch
Keyword(s):  
Caenorhabditis Elegans ◽  
Cell Volume Regulation ◽  
Ammonia Excretion ◽  
Transport Processes ◽  
Soil Nematode ◽  
Acid Base Balance ◽  
Nematode Caenorhabditis Elegans ◽  
Acid Base ◽  
C Elegans ◽  
Base Balance

Cation/proton exchangers of the cation proton antiporter 1 (CPA1) subfamily (NHEs, SLC 9) play an important role in many physiological processes, including cell volume regulation, acid–base homeostasis, and ammonia excretion. The soil nematode Caenorhabditis elegans (Maupas, 1900) (N2, 1968) expresses nine paralogues (NHX-1 to NHX-9). The current study was undertaken to investigate the role of the cation/proton exchanger in hypodermal Na+ and H+ fluxes, as well in ammonia excretion processes. Measurements using SIET (scanning ion-selective electrode technique) showed that the hypodermis promotes H+ secretion and Na+ uptake. Inhibitory effects on fluxes were observed upon application of amiloride but not EIPA, suggesting that NHXs are not involved in the transport processes. In response to stress induced by starvation or exposure to 1 mmol·L−1 NH4Cl, pH 5.5, or pH 8.0, body pH stayed fairly constant, with changes in mRNA expression levels detected in intestinal NHX-2 and hypodermal NHX-3. In conclusion, the study suggest that hypodermal apically localized EIPA-sensitive Na+/H+ exchangers do not likely play a role in ammonia excretion and Na+ uptake in the hypodermis of C. elegans, whereas apical amiloride-sensitive Na+ channels seem to be involved not just in hypodermal Na+ uptake but indirectly also in NH4+ and H+ excretion.

scholarly journals Mechanisms of acid–base regulation in seawater-acclimated green crabs (Carcinus maenas)

2016 ◽  
Vol 94 (2) ◽  
pp. 95-107 ◽  
Author(s):  
S. Fehsenfeld ◽  
D. Weihrauch
Keyword(s):  
Carbonic Anhydrase ◽  
Brackish Water ◽  
Carcinus Maenas ◽  
Ammonia Excretion ◽  
Respiratory Acidosis ◽  
Regulatory Mechanisms ◽  
Gill Epithelium ◽  
Acid Base ◽  
Bicarbonate Transporter ◽  
Bicarbonate Transporters

The present study investigated acid–base regulatory mechanisms in seawater-acclimated green crabs (Carcinus maenas (L., 1758)). In full-strength seawater, green crabs are osmoconformers so that the majority of the observed responses were attributed to ion fluxes based on acid–base compensatory responses alone. Similar to observations in brackish-water-acclimated C. maenas, seawater-acclimated green crabs exposed to hypercapnia rapidly accumulated HCO3− in their hemolymph, compensating for the respiratory acidosis caused by excess hemolymph pCO2. A full recovery from the decreased hemolymph pH after 48 h, however, was not observed. Gill perfusion experiments on anterior gill No. 5 indicated the involvement of all investigated genes (i.e., bicarbonate transporters, V-(H+)-ATPase, Na+/K+-ATPase, K+-channels, Na+/H+-exchanger, and carbonic anhydrase) in the excretion of acid–base equivalents. The most significant effects were observed when targeting a potentially cytoplasmic and (or) basolaterally localized V-(H+)-ATPase, as well as potentially basolaterally localized bicarbonate transporter (likely a Na+/HCO3−-cotransporter). In both cases, H+ accumulated in the hemolymph and CO2 excretion across the gill epithelium was significantly reduced or even reversed when blocking bicarbonate transporters. Based on the findings in this study, a working model for acid–base regulatory mechanisms and their link to ammonia excretion in the gill epithelium of C. maenas has been developed.

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