Role of Adrenal Steroids in Stimulating Ammonium Excretion during Acute Metabolic Acidosis

1997 ◽  
pp. 55-61
Author(s):  
P.J. Nolan ◽  
M.A. Knepper ◽  
R.K. Packer
Keyword(s):  
Metabolic Acidosis ◽  
Ammonium Excretion ◽  
Adrenal Steroids ◽  
Acute Metabolic Acidosis

scholarly journals Prompt Rise in Urinary Ammonium Excretion Suffices To Mitigate Metabolic Acidosis in an Experimental Animal Model of Severe Normovolemic Hemodilution

2017 ◽  
pp. 615-620 ◽  
Author(s):  
J. K. TELOH ◽  
I. N. WAACK ◽  
H. DE GROOT
Keyword(s):  
Metabolic Acidosis ◽  
Absolute Amount ◽  
Ammonium Excretion ◽  
Acid Excretion ◽  
Urinary Ph ◽  
Normovolemic Hemodilution ◽  
Proton Excretion ◽  
Acute Metabolic Acidosis ◽  
Experimental Group ◽  
Hasselbalch Equation

Recently, we have established a model of severe stepwise normovolemic hemodilution to a hematocrit of 10 % in rats employing three different colloidal volume replacement solutions (Voluven, Volulyte and Gelafundin) that are routinely used in clinical practice at present. We did not see severe dilutional acidosis as to be expected, but a decline in urinary pH. We here looked on further mechanisms of renal acid excretion during normovolemic hemodilution. Bicarbonate, which had been removed during normovolemic hemodilution, was calculated with the help of the Henderson-Hasselbalch equation. The urinary amount of ammonium as well as phosphate was determined in residual probes. The absolute amount of free protons in urine was obtained from the pH of the respective samples. The amount of protons generated during normovolemic hemodilution was approximately 0.6 mmol. During experimental time (5.5 h), distinct urinary ammonium excretion occurred (Voluven 0.52 mmol, Volulyte 0.39 mmol and Gelafundin 0.77 mmol). Proton excretion via the phosphate buffer constituted 0.04 mmol in every experimental group. Excretion of free protons was in the range of 10-6 mmol. The present data prove that the prompt rise in urinary ammonium excretion is also valid for acute metabolic acidosis originating from severe normovolemic hemodilution.

Importance of medullary events in ammonium excretion: studies in acute respiratory and acute metabolic acidosis

1983 ◽  
Vol 61 (1) ◽  
pp. 35-42 ◽  
Author(s):  
Andre Gougoux ◽  
Patrick Vinay ◽  
Guy Lemieux ◽  
Marc Goldstein ◽  
Bobby Stinebaugh ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Collecting Duct ◽  
Respiratory Acidosis ◽  
Renal Medulla ◽  
Hydrogen Ion ◽  
Ammonium Excretion ◽  
Urine Ph ◽  
Ion Secretion ◽  
Medullary Collecting Duct ◽  
Acute Metabolic Acidosis

The renal medulla can play an important role in acid excretion by modulating both hydrogen ion secretion in the medullary collecting duct and the medullary [Formula: see text]. The purpose of these experiments was to characterize the intrarenal events associated with ammonium excretion in acute acidosis. Cortical events were monitored in two ways: first, the rates of glutamine extraction and ammoniagenesis were assessed by measuring arteriovenous differences and the rate of renal blood flow; second, the biochemical response of the ammoniagenesis pathway was examined by measuring glutamate and 2-oxoglutarate, key renal cortical metabolites in this pathway. There were no significant differences noted in any of these cortical parameters between acute respiratory and metabolic acidosis. Despite a comparable twofold rise in ammonium excretion in both cases, the urine pH, [Formula: see text], and the urine minus blood [Formula: see text] difference (U-B [Formula: see text]) were lower during acute hypercapnia. In these experiments, the urine [Formula: see text] was 34 mmHg (1 mmHg = 133.322 Pa) lower than that of the blood during acute respiratory acidosis while the U-B [Formula: see text] was 5 ± 3 mmHg in acute metabolic acidosis. Thus there were significant differences in medullary events during these two conditions. Although the urine pH is critical in determining ammonium excretion in certain circumstances, these results suggest that regional variations in the medullary [Formula: see text] can modify this relationship.

Skeletal buffering of acute metabolic acidosis

1975 ◽  
Vol 229 (6) ◽  
pp. 1618-1624 ◽  
Author(s):  
JA Bettice ◽  
Gamble JL
Keyword(s):  
Metabolic Acidosis ◽  
Soft Tissue ◽  
Sodium Content ◽  
Long Bones ◽  
Exchangeable Sodium ◽  
Acid Infusion ◽  
Bone Water ◽  
Acute Metabolic Acidosis

Decreases in the sodium content of bone were measured to evaluate the role of this tissue in the buffering of acute metabolic acidosis. The bones of rats and dogs were labeled with radiosodium prior to the infusion of HCl, and changes in the radioactivity were used to indicate the loss of bone sodium. Significant reductions in the skeletal sodium occurred within the first 5 h of acidosis, and these losses can only be partially attributed to the hyponatremia accompanying the acid infusion. Decreases were greatest in the smaller bones of the rat; and, in the dog, the losses from flat bones exceeded those of the long bones. Only the rapidly exchangeable sodium of bone was involved in the changes due to acidosis. Soft tissue buffering may be more important initially; during 1.5-h experiments, the skeletal losses were small and could be ascribed almost entirely to the decrease in the amount of sodium contained in bone water. However, at the end of 5.0 h, the quantity of sodium released from the skeleton is sufficient to account for much of the tissue buffering.

Role of acidosis-induced increases in calcium on PTH secretion in acute metabolic and respiratory acidosis in the dog

2004 ◽  
Vol 286 (5) ◽  
pp. E780-E785 ◽  
Author(s):  
Ignacio López ◽  
Escolástico Aguilera-Tejero ◽  
José Carlos Estepa ◽  
Mariano Rodríguez ◽  
Arnold J. Felsenfeld
Keyword(s):  
Parathyroid Hormone ◽  
Metabolic Acidosis ◽  
Specific Effect ◽  
Respiratory Acidosis ◽  
Normal Value ◽  
Baseline Values ◽  
Acute Metabolic Acidosis ◽  
Sufficient Magnitude ◽  
Edta Infusion

Recently, we showed that both acute metabolic acidosis and respiratory acidosis stimulate parathyroid hormone (PTH) secretion in the dog. To evaluate the specific effect of acidosis, ionized calcium (iCa) was clamped at a normal value. Because iCa values normally increase during acute acidosis, we now have studied the PTH response to acute metabolic and respiratory acidosis in dogs in which the iCa concentration was allowed to increase (nonclamped) compared with dogs with a normal iCa concentration (clamped). Five groups of dogs were studied: control, metabolic (clamped and nonclamped), and respiratory (clamped and nonclamped) acidosis. Metabolic (HCl infusion) and respiratory (hypoventilation) acidosis was progressively induced during 60 min. In the two clamped groups, iCa was maintained at a normal value with an EDTA infusion. Both metabolic and respiratory acidosis increased ( P < 0.05) iCa values in nonclamped groups. In metabolic acidosis, the increase in iCa was progressive and greater ( P < 0.05) than in respiratory acidosis, in which iCa increased by 0.04 mM and then remained constant despite further pH reductions. The increase in PTH values was greater ( P < 0.05) in clamped than in nonclamped groups (metabolic and respiratory acidosis). In the nonclamped metabolic acidosis group, PTH values first increased and then decreased from peak values when iCa increased by >0.1 mM. In the nonclamped respiratory acidosis group, PTH values exceeded ( P < 0.05) baseline values only after iCa values stopped increasing at a pH of 7.30. For the same increase in iCa in the nonclamped groups, PTH values increased more in metabolic acidosis. In conclusion, 1) both metabolic acidosis and respiratory acidosis stimulate PTH secretion; 2) the physiological increase in the iCa concentration during the induction of metabolic and respiratory acidosis reduces the magnitude of the PTH increase; 3) in metabolic acidosis, the increase in the iCa concentration can be of sufficient magnitude to reverse the increase in PTH values; and 4) for the same degree of acidosis-induced hypercalcemia, the increase in PTH values is greater in metabolic than in respiratory acidosis.

Effect of acidosis on PTH-dependent renal adenylate cyclase in phosphorus deprivation: role of G proteins

1990 ◽  
Vol 258 (6) ◽  
pp. F1640-F1649
Author(s):  
E. Bellorin-Font ◽  
R. Starosta ◽  
C. L. Milanes ◽  
C. Lopez ◽  
N. Pernalete ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Adenylate Cyclase ◽  
Maximal Activity ◽  
Phosphate Deprivation ◽  
Adp Ribosylation ◽  
Phosphate Depletion ◽  
Cortical Membranes ◽  
And Function ◽  
Gs Alpha

These studies examine the regulation of adenylate cyclase in renal cortical membranes from phosphate-deprived and phosphate-deprived acidotic dogs. Enzyme stimulation by parathyroid hormone (PTH) was decreased in phosphate deprivation [Vmax 1,578 +/- 169 vs. 2,581 +/- 219 pmol adenosine 3',5'-cyclic monophosphate (cAMP).mg protein-1 x 30 min-1 in controls, P less than 0.01]. Metabolic acidosis further decreased PTH-stimulated activity. Membranes from phosphate-deprived dogs showed a decrease in Gs alpha-content by cholera toxin-dependent ADP-ribosylation (174 +/- 18 arbitrary units vs. 266.4 +/- 13.6 in controls, P less than 0.01). Metabolic acidosis further decreased Gs alpha-content, P less than 0.01. Gi content by pertussis-dependent ADP-ribosylation was also lower in phosphate-deprived and phosphate-deprived acidotic animals. Gs function was examined by its property to protect the catalytic unit from inactivation by N-ethylmaleimide when preincubated with GTP gamma S. In controls, protection of inactivation was 80% of the maximal activity, whereas in phosphate deprivation protection was less than 50%. In conclusion, metabolic acidosis enhances adenylate cyclase resistance to PTH in phosphate deprivation. These alterations are associated with a decrease in the content and function of Gs alpha, suggesting a role of Gs in the renal adaptation to phosphate depletion and acidosis.

The renin-angiotensin system in kidney development: role of COX-2 and adrenal steroids

2004 ◽  
Vol 181 (4) ◽  
pp. 549-559 ◽  
Author(s):  
B. L. Jensen ◽  
J. Stubbe ◽  
K. Madsen ◽  
F. T. Nielsen ◽  
O. Skott
Keyword(s):  
Kidney Development ◽  
Renin Angiotensin System ◽  
Adrenal Steroids ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Cox 2
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