Effects of Acute Acid–Base Alterations on Glutamine Metabolism and Renal Ammoniagenesis in the Dog

1978 ◽  
Vol 54 (5) ◽  
pp. 503-508 ◽  
Author(s):  
A. Fine ◽  
F. I. Bennett ◽  
G. A. O. Alleyne

1. The effects of acute acid—base alterations on renal ammonia production and glutamine metabolism were studied in anaesthetized dogs. 2. Plasma glutamine rose with acidosis and also when both Pco2 and plasma HCO−3 were raised isohydrically. 3. Blood urea fell when acidosis was induced with hydrochloric acid. 4. The renal production of ammonia per ml of renal blood flow was increased in acidosis, but this was independent of the amount of glutamine delivered to the kidney. 5. The results indicate that acute acidosis affects production of urea and glutamine and increases the capacity of the renal cells to extract glutamine from blood.

2020 ◽  
Vol 319 (6) ◽  
pp. F1081-F1089
Author(s):  
Andrew R. Steele ◽  
Michael M. Tymko ◽  
Victoria L. Meah ◽  
Lydia L. Simpson ◽  
Christopher Gasho ◽  
...  

Early acclimatization to high altitude is characterized by various respiratory, hematological, and cardiovascular adaptations that serve to restore oxygen delivery to tissue. However, less is understood about renal function and the role of renal oxygen delivery (RDO2) during high altitude acclimatization. We hypothesized that 1) RDO2 would be reduced after 12 h of high altitude exposure (high altitude day 1) but restored to sea level values after 1 wk (high altitude day 7) and 2) RDO2 would be associated with renal reactivity, an index of acid-base compensation at high altitude. Twenty-four healthy lowlander participants were tested at sea level (344 m, Kelowna, BC, Canada) and on day 1 and day 7 at high altitude (4,330 m, Cerro de Pasco, Peru). Cardiac output, renal blood flow, and arterial and venous blood sampling for renin-angiotensin-aldosterone system hormones and NH2-terminal pro-B-type natriuretic peptides were collected at each time point. Renal reactivity was calculated as follows: (Δarterial bicarbonate)/(Δarterial Pco2) between sea level and high altitude day 1 and sea level and high altitude day 7. The main findings were that 1) RDO2 was initially decreased at high altitude compared with sea level (ΔRDO2: −22 ± 17%, P < 0.001) but was restored to sea level values on high altitude day 7 (ΔRDO2: −6 ± 14%, P = 0.36). The observed improvements in RDO2 resulted from both changes in renal blood flow (Δ from high altitude day 1: +12 ± 11%, P = 0.008) and arterial oxygen content (Δ from high altitude day 1: +44.8 ± 17.7%, P = 0.006) and 2) renal reactivity was positively correlated with RDO2 on high altitude day 7 ( r = 0.70, P < 0.001) but not high altitude day 1 ( r = 0.26, P = 0.29). These findings characterize the temporal responses of renal function during early high altitude acclimatization and the influence of RDO2 in the regulation of acid-base balance.


1987 ◽  
Vol 72 (1) ◽  
pp. 61-69 ◽  
Author(s):  
Jorge Areas ◽  
Sevag Balian ◽  
Dianna Slemmer ◽  
Mario Belledonne ◽  
Harry G. Preuss

1. Adaptation of renal ammoniagenesis during acute metabolic acidosis in intact dogs may be nonexistent or, at least, markedly less than in chronic acidosis. This contrasts to adaptation in acute respiratory acidosis, where levels similar to those attained in chronic acidosis occur within hours. 2. Accordingly, the inability to discern marked changes in acute metabolic acidosis compared with acute respiratory acidosis has been attributed to decreased glomerular filtration rate and renal blood flow seen frequently in the former. 3. In our studies, we found early changes in ammoniagenesis and glutamine metabolism during acute metabolic acidosis, but not of the magnitude seen in chronic acidosis, even considering the changes in renal blood flow (RBF) and glomerular filtration rate (GFR). Exogenous glutamine loading allowed us to discover that the qualitative changes in glutamine metabolism during acute metabolic acidosis differed from control but fell short of those seen in chronic metabolic a acidosis. 4. We also examined glutamine metabolism when renal ammoniagenic adaptation was acutely inhibited in chronically acidotic dogs. Infusing NaHCO3 into chronically acidotic dogs decreased renal ammonia production significantly (247 μmol min−1 100 ml−1 GFR vs 148 μmol min−1 100 ml−1 GFR: P < 0.001) and glutamine extraction (111.8 μmol min−1 100 ml−1 GFR vs 90.9 μmol min−1 100 ml−1 GFR: P < 0.02). 5. The qualitative changes in renal glutamine metabolism in both studies suggest that alterations in deamination of glutamate formed from glutamine are responsible, at least in part, for adaptation to acute acid–base perturbations. 6. Compared with respiratory acidosis, adaptation to metabolic acidosis is progressive and prolonged.


1982 ◽  
Vol 243 (3) ◽  
pp. F227-F234
Author(s):  
A. Gougoux ◽  
P. Vinay ◽  
M. Cardoso ◽  
M. Duplain ◽  
G. Lemieux

Studies were performed to determine whether ammoniagenesis could adapt instantaneously to acidosis in the dog kidney. Following acute respiratory acidosis, renal glutamine extraction rose acutely in dogs with stable renal blood flow but did not change when the renal blood flow fell by more than 25%. Acute hypercapnia immediately increased renal ammonia production in both groups of dogs. The rate of both glutamine extraction and ammonia production in acutely hypercapnic dogs without hemodynamic changes was comparable to the rates observed in dogs with chronic metabolic acidosis. Furthermore, the renal metabolite profile observed in acute hypercapnia was similar to the pattern described in chronic metabolic acidosis, i.e., a marked fall in renal glutamate and alpha-ketoglutarate concentrations and a fivefold increase in malate and oxaloacetate concentrations. In the liver and muscle, acute hypercapnia induced no significant change in glutamine concentration but glutamate and alpha-ketoglutarate concentrations decreased. Our findings demonstrate that the dog kidney can adapt immediately to acidosis but that hemodynamic change may mask this adaptation.


1978 ◽  
Vol 38 (5) ◽  
pp. 495-499 ◽  
Author(s):  
Torbjörn Leivestad ◽  
Erling Brodwall ◽  
Svein Simonsen

1990 ◽  
Vol 31 (5) ◽  
pp. 538-539
Author(s):  
G. M. Cleator ◽  
P. E. Klapper ◽  
A. G. Lewis ◽  
H. L. Sharma ◽  
A. M. Smith

Author(s):  
Bashair A. Alhummiany ◽  
David Shelley ◽  
Margaret Saysell ◽  
Maria‐Alexandra Olaru ◽  
Bernd Kühn ◽  
...  

2000 ◽  
Vol 279 (4) ◽  
pp. R1268-R1276 ◽  
Author(s):  
Paul P. Leyssac ◽  
Niels-Henrik Holstein-Rathlou ◽  
Ole Skøtt

Inconsistencies in previous reports regarding changes in early distal NaCl concentration (EDNaCl) and renin secretion during osmotic diuresis motivated our reinvestigation. After intravenous infusion of 10% mannitol, EDNaCl fell from 42.6 to 34.2 mM. Proximal tubular pressure increased by 12.6 mmHg. Urine flow increased 10-fold, and sodium excretion increased by 177%. Plasma renin concentration (PRC) increased by 58%. Renal blood flow and glomerular filtration rate decreased, however end-proximal flow remained unchanged. After a similar volume of hypotonic glucose (152 mM), EDNaClincreased by 3.6 mM, ( P < 0.01) without changes in renal hemodynamics, urine flow, sodium excretion rate, or PRC. Infusion of 300 μmol NaCl in a smaller volume caused EDNaCl to increase by 6.4 mM without significant changes in PRC. Urine flow and sodium excretion increased significantly. There was a significant inverse relationship between superficial nephron EDNaCl and PRC. We conclude that EDNa decreases during osmotic diuresis, suggesting that the increase in PRC was mediated by the macula densa. The results suggest that the natriuresis during osmotic diuresis is a result of impaired sodium reabsorption in distal tubules and collecting ducts.


1979 ◽  
Vol 84 (2) ◽  
pp. 163-171 ◽  
Author(s):  
A.-C. Ericson ◽  
M. Sjöquist ◽  
H. R. Ulfendahl

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