Inner medullary collecting duct function during rebound alkalemia

1987 ◽  
Vol 252 (4) ◽  
pp. F712-F716
Author(s):  
H. H. Bengele ◽  
E. R. McNamara ◽  
J. H. Schwartz ◽  
E. A. Alexander
Keyword(s):  
Collecting Duct ◽  
Acid Excretion ◽  
Acid Base ◽  
Proton Secretion ◽  
Inner Medullary Collecting Duct ◽  
Titratable Acid ◽  
Base Parameters ◽  
Arterial Ph ◽  
Medullary Collecting Duct ◽  
Net Acid Excretion

Rats, made acidemic when fed NH4Cl, become alkalemic with discontinuation of the NH4Cl. This phenomenon has been called rebound metabolic alkalemia (RMA). This study examines the function of the inner medullary collecting duct (IMCD) during RMA. Rats drank only 1.5% NH4Cl for 5 days and then water for 16 h prior to study, yielding an arterial pH = 7.50 +/- 0.01, PCO2 = 39 +/- 1 mmHg, and bicarbonate = 29.5 +/- 1.0 mM. The IMCD data were obtained by microcatheterization from deep (1.5-3.0 mm) and tip (0.2-0.5 mm) samples. Equilibrium pH decreased from 5.92 +/- 0.09 (n = 20) to 5.38 +/- 0.04 (n = 20) and PCO2 increased from 32 +/- 1 to 38 +/- 1 mmHg between deep and tip samples. Bicarbonate delivery decreased from 37 +/- 8 to 7 +/- 1 nmol/min. Titratable acid and ammonium delivery increased from 284 +/- 52 to 347 +/- 62 nmol/min and from 549 +/- 38 to 685 +/- 40 nmol/min, respectively. Calculated net acid excretion increased from 796 +/- 88 to 1,026 +/- 95 nmol/min. Thus during RMA, proton secretion continues along the IMCD, although there is a systemic alkalemia. It appears that factors in addition to systemic acid-base parameters are important in the regulation of proton secretion by the IMCD.

Effect of buffer infusion during acute respiratory acidosis

1986 ◽  
Vol 250 (1) ◽  
pp. F115-F119 ◽  
Author(s):  
H. H. Bengele ◽  
J. H. Schwartz ◽  
E. R. McNamara ◽  
E. A. Alexander
Keyword(s):  
Collecting Duct ◽  
Respiratory Acidosis ◽  
Membrane Electrodes ◽  
Proton Secretion ◽  
Inner Medullary Collecting Duct ◽  
Titratable Acid ◽  
Arterial Ph ◽  
Glass Membrane ◽  
Medullary Collecting Duct ◽  
Terminal Nephron

We previously reported that acute respiratory acidosis (ARA) did not stimulate inner medullary collecting duct (IMCD) acidification. It was possible that the failure to find enhanced IMCD acidification was a function of insufficient buffer delivery. To answer this question we studied IMCD acidification in rats with ARA during the infusion of the buffer creatinine. We employed the microcatheterization technique to directly measure pH and PCO2 with glass membrane electrodes and also obtained fluid samples for the measurement of titratable acid and ammonium. Arterial pH was 7.19 +/- 0.01 and PCO2 was 93 +/- 2 mmHg. The IMCD data were analyzed as a function of IMCD length (approximately 6 mm). Equilibrium pH decreased from 5.99 +/- 0.05 to 5.58 +/- 0.02 and PCO2 increased from 71 +/- 11 to 132 +/- 6 mmHg between origin and tip. Bicarbonate delivery decreased from 111 +/- 14 to 38 +/- 2 nmol/min; titratable acid increased from 867 +/- 87 to 1,625 +/- 61 nmol/min, but ammonium delivery did not change along the duct. Thus, estimated net acid increased from 1,772 +/- 155 to 2,709 +/- 88 nmol/min. We conclude that during the presence of increased buffer delivery to the IMCD, rats with ARA markedly increased proton secretion along the terminal nephron.

Acidification adaptation along the inner medullary collecting duct

1988 ◽  
Vol 255 (6) ◽  
pp. F1155-F1159 ◽  
Author(s):  
H. H. Bengele ◽  
E. R. McNamara ◽  
J. H. Schwartz ◽  
E. A. Alexander
Keyword(s):  
Acid Secretion ◽  
Collecting Duct ◽  
Acid Base ◽  
Regular Diet ◽  
Inner Medullary Collecting Duct ◽  
Titratable Acid ◽  
Arterial Ph ◽  
Acid Base Status ◽  
Medullary Collecting Duct ◽  
Additional Support

Chronic acid feeding (ACD) stimulates and chronic alkali (AKL) feeding suppresses acid secretion along the inner medullary collecting duct (IMCD) of the rat. The purpose of these experiments was to determine whether these stimuli produce IMCD acidification adaptation. We tested this hypothesis by acutely changing systemic PCO2 in rats chronically fed ACD or ALK. Microcatheterization was used to measure pH and PCO2 and samples were simultaneously obtained for measurement of bicarbonate, titratable acid (TA), and ammonium. In 10 ACD rats (arterial pH, 7.26 +/- 0.01; PCO2, 88 +/- 1 mmHg) acid secretion along the IMCD was 506 +/- 88 nmol/min. In 10 ALK rats with similar arterial gases (pH, 7.16 +/- 0.02; PCO2, 82 +/- 1 mmHg) IMCD acid secretion was only 284 +/- 57 nmol/min, P less than 0.05. In ACD rats made hypocarbic (pH, 7.26 +/- 0.03; PCO2, 24 +/- 1 mmHg), IMCD acid secretion was 163 +/- 55 nmol/min. These data were compared with previously studied rats eating a regular diet. Acute hypocarbia (pH, 7.54 +/- 0.02; PCO2, 20 +/- 1 mmHg) completely suppressed acid secretion, 4 +/- 23 nmol/min, along the IMCD. We conclude that chronic alterations in acid-base status provide an IMCD "set" where comparable stimuli produce significant differences in IMCD acidification. These data provide additional support for the concept of IMCD acidification adaptation.

Suppression of acidification along inner medullary collecting duct

1988 ◽  
Vol 255 (2) ◽  
pp. F307-F312 ◽  
Author(s):  
H. H. Bengele ◽  
E. R. McNamara ◽  
J. H. Schwartz ◽  
E. A. Alexander
Keyword(s):  
Acid Secretion ◽  
Collecting Duct ◽  
Respiratory Alkalosis ◽  
Inner Medullary Collecting Duct ◽  
Titratable Acid ◽  
Arterial Ph ◽  
Medullary Collecting Duct ◽  
Collection Sites

The purpose of these experiments was to evaluate the effect of acute respiratory alkalosis (ARA) and chronic bicarbonate drinking (CBD) on inner medullary collecting duct (IMCD) acidification. Microcatheterization was used to measure pH and PCO2, and samples were simultaneously obtained for measurement of bicarbonate, titratable acid (TA), and ammonium. In ten ARA rats (arterial pH was 7.54 +/- 0.02; PCO2 was 20 +/- 1 mmHg), IMCD equilibrium pH was not different (deep pH was 5.65 +/- 0.06 and PCO2 was 20 +/- 1 mmHg; tip pH was 5.54 +/- 0.07 and PCO2 was 22 +/- 1 mmHg). Delivery of bicarbonate, TA, and ammonium also did not differ between collection sites. Thus net acidification along the IMCD was negligible. Nine rats drank NaHCO3 for 5-8 days (pH = 7.48 +/- 0.02) but did not receive NaHCO3 during the experiment so that arterial pH fell to 7.40 +/- 0.01. IMCD equilibrium pH was different at deep (pH was 5.68 +/- 0.06; PCO2 was 32 +/- 1 mmHg) and tip (pH was 5.57 +/- 0.04; PCO2 was 27 +/- 1 mmHg; P less than or equal to 0.05) collection sites. However, only minimal changes in the delivery of bicarbonate, TA, and ammonium were noted, and net acidification along the IMCD was negligible. In ten control rats, net acidification was 219 nmol/min between collection sites (P less than 0.001). We conclude that ARA and CBD abolish acidification along the IMCD. In addition, CBD produces an intrinsic modification along the IMCD, which suppresses acid secretion and persists after acute recovery from alkalemia.

Effect of acute thyroparathyroidectomy on nephron acidification

1984 ◽  
Vol 246 (5) ◽  
pp. F569-F574 ◽  
Author(s):  
H. H. Bengele ◽  
E. R. McNamara ◽  
E. A. Alexander
Keyword(s):  
Parathyroid Hormone ◽  
Proximal Tubule ◽  
Collecting Duct ◽  
Distal Tubule ◽  
Acid Excretion ◽  
Acid Phosphate ◽  
Inner Medullary Collecting Duct ◽  
Medullary Collecting Duct ◽  
Net Acid Excretion

The effect of the absence of parathyroid hormone on nephron acidification was determined in rats after acute thyroparathyroidectomy (TPTX). Tubular fluid samples were obtained from the superficial late proximal tubule (LPT), the early distal tubule ( EDT ), and along the inner medullary collecting duct (IMCD), and the results were compared with those obtained from control rats. In the LPT after TPTX, pH was lower, 6.66 +/- 0.01 vs. 6.73 +/- 0.01, and ammonium and net acid delivery were increased significantly. In the EDT no differences in pH, bicarbonate, or net acid were found between groups, whereas ammonium and acid phosphate were significantly different. Along the IMCD in control rats, pH decreased from 6.58 to 5.21 and the addition of about 430 nmol/min of net acid was observed. After TPTX more net acid entered the duct and pH was lower, 5.66, but did not change; neither did the amount of bicarbonate, ammonium, acid phosphate, or net acid change significantly along the duct. Net acid excretion was not different, however, among groups. These results demonstrate that TPTX markedly affects nephron acidification, increasing net acid along the proximal tubule. In contrast to that in control rats, however, net acidification is completed prior to the IMCD. We conclude that the acute absence of parathyroid hormone may significantly affect local nephron acidification but does not alter acid excretion.

Chronic metabolic acidosis augments acidification along the inner medullary collecting duct

1986 ◽  
Vol 250 (4) ◽  
pp. F690-F694 ◽  
Author(s):  
H. H. Bengele ◽  
J. H. Schwartz ◽  
E. R. McNamara ◽  
E. A. Alexander
Keyword(s):  
Metabolic Acidosis ◽  
Acid Secretion ◽  
Ammonium Chloride ◽  
Collecting Duct ◽  
Major Site ◽  
Chronic Metabolic Acidosis ◽  
Inner Medullary Collecting Duct ◽  
Titratable Acid ◽  
Arterial Ph ◽  
Medullary Collecting Duct

The inner medullary collecting duct (IMCD) of the rat is a major site of acidification. However, previous micropuncture studies have failed to demonstrate acidification along the terminal IMCD during chronic acid feeding. To more completely evaluate this question we used the microcatheterization method in rats fed ammonium chloride for 3-7 days. Arterial pH was 7.30 +/- 0.015, and PCO2 was set at 40 +/- 0.6 mmHg. The IMCD data were analyzed as a function of IMCD length between 40% and the tip. Equilibrium pH decreased from 6.21 +/- 0.11 to 5.47 +/- 0.03, whereas PCO2 was unchanged (28 +/- 1 mmHg between the deep samples and tip). Bicarbonate delivery decreased from 92 +/- 14 to 10 +/- 1 nmol/min, titratable acid increased from 462 +/- 33 to 762 +/- 40 nmol/min, and ammonium delivery increased from 2,235 +/- 121 to 3,528 +/- 140 nmol/min. Thus estimated net acid increased from 2,638 +/- 134 to 4,303 +/- 161 nmol/min. To determine whether increasing delivery of buffer to the IMCD would stimulate acid secretion in acute acidosis, rats were studied during the infusion of HCl and creatinine. Arterial pH was 7.18 +/- 0.02. IMCD acidification was not increased compared with our previously published studies during HCl infusion [Am. J. Physiol. 241 (Renal Fluid Electrolyte Physiol. 10): F669-F676, 1981]. We conclude that chronic ammonium chloride ingestion stimulates IMCD acidification and that this increase may be an intrinsic modification of the acidification mechanism of the IMCD.

Pendrin in the mouse kidney is primarily regulated by Cl− excretion but also by systemic metabolic acidosis

2008 ◽  
Vol 295 (6) ◽  
pp. C1658-C1667 ◽  
Author(s):  
Patricia Hafner ◽  
Rosa Grimaldi ◽  
Paola Capuano ◽  
Giovambattista Capasso ◽  
Carsten A. Wagner
Keyword(s):  
Metabolic Acidosis ◽  
Collecting Duct ◽  
Relative Number ◽  
High Protein ◽  
Acid Excretion ◽  
Acid Base ◽  
Urinary Acidification ◽  
Apical Side ◽  
Acid Base Status ◽  
Net Acid Excretion

The Cl−/anion exchanger pendrin (SLC26A4) is expressed on the apical side of renal non-type A intercalated cells. The abundance of pendrin is reduced during metabolic acidosis induced by oral NH4Cl loading. More recently, it has been shown that pendrin expression is increased during conditions associated with decreased urinary Cl− excretion and decreased upon Cl− loading. Hence, it is unclear if pendrin regulation during NH4Cl-induced acidosis is primarily due the Cl− load or acidosis. Therefore, we treated mice to increase urinary acidification, induce metabolic acidosis, or provide an oral Cl− load and examined the systemic acid-base status, urinary acidification, urinary Cl− excretion, and pendrin abundance in the kidney. NaCl or NH4Cl increased urinary Cl− excretion, whereas (NH4)2SO4, Na2SO4, and acetazolamide treatments decreased urinary Cl− excretion. NH4Cl, (NH4)2SO4, and acetazolamide caused metabolic acidosis and stimulated urinary net acid excretion. Pendrin expression was reduced under NaCl, NH4Cl, and (NH4)2SO4 loading and increased with the other treatments. (NH4)2SO4 and acetazolamide treatments reduced the relative number of pendrin-expressing cells in the collecting duct. In a second series, animals were kept for 1 and 2 wk on a low-protein (20%) diet or a high-protein (50%) diet. The high-protein diet slightly increased urinary Cl− excretion and strongly stimulated net acid excretion but did not alter pendrin expression. Thus, pendrin expression is primarily correlated with urinary Cl− excretion but not blood Cl−. However, metabolic acidosis caused by acetazolamide or (NH4)2SO4 loading prevented the increase or even reduced pendrin expression despite low urinary Cl− excretion, suggesting an independent regulation by acid-base status.

Effect of respiratory acidosis on acidification by the medullary collecting duct

1983 ◽  
Vol 244 (1) ◽  
pp. F89-F94 ◽  
Author(s):  
H. H. Bengele ◽  
M. L. Graber ◽  
E. A. Alexander
Keyword(s):  
Collecting Duct ◽  
Respiratory Acidosis ◽  
Hydrogen Ion ◽  
Membrane Electrodes ◽  
Acid Excretion ◽  
Acid Phosphate ◽  
Arterial Ph ◽  
Glass Membrane ◽  
Medullary Collecting Duct ◽  
Acute Metabolic Acidosis

The effect of acute respiratory acidosis (ARA) on inner medullary collecting duct (IMCD) acidification was studied and the results were compared with previously obtained data by our laboratory in rats with acute metabolic acidosis (AMA). We employed the microcatheterization technique to directly measure pH and PCO2 with glass-membrane electrodes, and fluid samples were obtained for measurement of bicarbonate, phosphate, and ammonium. Arterial pH was 7.18 +/- 0.01 and PCO2 was 88 +/- 2 mmHg. The IMCD data were analyzed as a function of IMCD length (approximately 6 mm). pH decreased from 5.78 +/- 0.07 to 5.27 +/- 0.03 and PCO2 increased from 55 +/- 4 to 75 +/- 2 mmHg between origin and tip. Bicarbonate delivery decreased from 154 +/- 34 to 25 +/- 3 nmol/min but no change was noted in acid phosphate, ammonium, or net acid addition along the IMCD. However, net acid excretion was not different from that found previously in AMA. We conclude that during ARA acidification is augmented prior to, but not along, the IMCD. In contrast, during AMA we previously found that IMCD plays a major regulatory role in urinary acidification, accounting for about 50% of the excreted hydrogen ion.

scholarly journals Ammonia Transporters and Their Role in Acid-Base Balance

2017 ◽  
Vol 97 (2) ◽  
pp. 465-494 ◽  
Author(s):  
I. David Weiner ◽  
Jill W. Verlander
Keyword(s):  
Ammonia Excretion ◽  
Transport Processes ◽  
Molecular Forms ◽  
Acid Excretion ◽  
Acid Base ◽  
Titratable Acid ◽  
Renal Net Acid Excretion ◽  
Ammonia Transport ◽  
Specific Proteins ◽  
Net Acid Excretion

Acid-base homeostasis is critical to maintenance of normal health. Renal ammonia excretion is the quantitatively predominant component of renal net acid excretion, both under basal conditions and in response to acid-base disturbances. Although titratable acid excretion also contributes to renal net acid excretion, the quantitative contribution of titratable acid excretion is less than that of ammonia under basal conditions and is only a minor component of the adaptive response to acid-base disturbances. In contrast to other urinary solutes, ammonia is produced in the kidney and then is selectively transported either into the urine or the renal vein. The proportion of ammonia that the kidney produces that is excreted in the urine varies dramatically in response to physiological stimuli, and only urinary ammonia excretion contributes to acid-base homeostasis. As a result, selective and regulated renal ammonia transport by renal epithelial cells is central to acid-base homeostasis. Both molecular forms of ammonia, NH3 and NH4+, are transported by specific proteins, and regulation of these transport processes determines the eventual fate of the ammonia produced. In this review, we discuss these issues, and then discuss in detail the specific proteins involved in renal epithelial cell ammonia transport.

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