Metabolic acid-base influences on renal thiazide receptor density

1997 ◽  
Vol 272 (6) ◽  
pp. R2004-R2008 ◽  
Author(s):  
D. D. Fanestil ◽  
D. A. Vaughn ◽  
P. Blakely
Keyword(s):  
Metabolic Acidosis ◽  
Hydrogen Ion ◽  
Loop Of Henle ◽  
Receptor Density ◽  
Distal Nephron ◽  
Acid Base ◽  
Collecting Ducts ◽  
Wistar Kyoto ◽  
Induced Changes ◽  
Renal Responses

The renal responses to metabolic acidosis/alkalosis involve changes in the proximal tubule, loop of Henle, and collecting ducts. We tested for acid- or base-induced changes in the distal convoluted tubule (DCT) by examining the renal density of the DCT's receptor for thiazide-type diuretics (TZR), as estimated by the binding of [3H]metolazone in Wistar-Kyoto rats. TZR density significantly decreased by 17% in rats ingesting NH4Cl for 3.5 days and by nearly 30% after 7 days; TZR increased up to 40% in rats ingesting NaHCO3 for 2-4 days but was no longer significantly increased after 7 days. Urinary excretion of chloride increased as renal density of the TZR decreased, a finding consistent with the interpretation that acidosis/alkalosis not only altered TZR density but coordinately altered reabsorption of NaCl by the thiazidesensitive Na-Cl cotransporter. The result is that delivery of Na from DCT is enhanced during acidosis and decreased during alkalosis, assisting in compensatory changes in distal nephron secretion of hydrogen ion. The integrated renal response to metabolic acidosis/alkalosis involves a decrease in renal TZR with acidosis and an increase in TZR with alkalosis.

Model explaining the relation between distal nephron Li+ reabsorption and urinary Na+ excretion in rats

1998 ◽  
Vol 274 (3) ◽  
pp. F445-F452 ◽  
Author(s):  
Michael Shalmi ◽  
Thomas Jonassen ◽  
Klaus Thomsen ◽  
Jonathan D. Kibble ◽  
Peter Bie ◽  
...  
Keyword(s):  
Urinary Excretion ◽  
Apical Membrane ◽  
Fractional Excretion ◽  
Distal Nephron ◽  
Conscious Rats ◽  
Angiotensin Iii ◽  
Collecting Ducts ◽  
Induced Changes ◽  
Different Levels

Li+ may be reabsorbed via an amiloride-sensitive mechanism in the collecting ducts of rats administered a low-Na+ diet. This was investigated by measuring the increase in fractional urinary excretion of Li+(FELi) in response to amiloride in conscious rats at two different levels of plasma Li+ concentration and after administration of bendroflumethiazide (BFTZ), angiotensin III (ANG III), and aldosterone (Aldo). The results confirmed that amiloride increased (FELi) in rats on a low-Na+ diet (20 ± 1 to 35 ± 1%, means ± SE), whereas no increase was observed in rats on a normal Na+ diet (37 ± 1 to 38 ± 1%). The lithiuretic effect of amiloride was 1) abolished by preadministration of BFTZ (32 ± 1 to 33 ± 2%) to Na+-deprived rats and 2) increased by ANG III (27 ± 3 to 33 ± 2%) and Aldo (25 ± 2 to 37 ± 2%) in Na+-replete rats. Amiloride-induced changes in FELiwere independent of plasma Li+concentration but inversely related to the fractional excretion of Na+ and the amiloride-sensitive excretion of K+. These results are compatible with the hypothesis that a low tubular Na+ concentration reduces end-tubular Na+ reabsorption and results in hyperpolarization of the apical membrane, thus favoring Li+ uptake into the cells.

Adaptive changes in renal acidification in response to chronic respiratory acidosis

1985 ◽  
Vol 248 (4) ◽  
pp. F492-F499 ◽  
Author(s):  
R. L. Tannen ◽  
B. Hamid
Keyword(s):  
Metabolic Acidosis ◽  
Proton Transport ◽  
Respiratory Acidosis ◽  
Hydrogen Ion ◽  
Distal Nephron ◽  
Urine Ph ◽  
Chronic Metabolic Acidosis ◽  
Adaptive Changes ◽  
Secretory Capacity

To examine whether chronic respiratory acidosis results in adaptive changes in renal acidification, rats were housed for 3 days in an environmental chamber with an ambient CO2 content of 10% and their kidneys were perfused in vitro according to two protocols. To assess hydrogen ion secretory capacity of the distal nephron, perfusions were carried out with a low bicarbonate concentration, in the absence of ammoniagenic substrate, and with saturating quantities of the buffer creatinine. Under these conditions, the titration of creatinine at a pH less than 6.0 (TA pH 6.0) reflects the H+ secretory capacity of a discrete functional segment of the distal nephron. Kidneys from rats with chronic respiratory acidosis exhibited a significantly lower urine pH and higher rate of TA pH 6.0 than controls perfused in this fashion, indicative of an adaptive increase in the distal nephron capacity for proton transport. This adaptation was comparable with that reported previously for rats exposed to chronic metabolic acidosis. Furthermore, evidence of adaptation persisted in the presence of amiloride (10(-5) M), suggesting that it reflects, at least in part, a sodium-independent mechanism of proton transport. Hydrogen ion secretion by the proximal nephron was assessed by performing standard bicarbonate titration curves with kidneys from rats with chronic respiratory acidosis, chronic metabolic acidosis, and controls using a perfusate equilibrated with 95% O2/5% CO2.(ABSTRACT TRUNCATED AT 250 WORDS)

A physiological approach to acid–base disorders: The roles of ion transport and body fluid compartments

2020 ◽  
pp. 2182-2198
Author(s):  
Julian Seifter
Keyword(s):  
Metabolic Acidosis ◽  
Gas Analysis ◽  
Hydrogen Ion ◽  
Anion Gap ◽  
Ion Concentration ◽  
Hydrogen Ions ◽  
Acid Base ◽  
Hydrogen Ion Concentration ◽  
Arterial Blood Gas ◽  
Fluid Compartments

The normal pH of human extracellular fluid is maintained within the range of 7.35 to 7.45. The four main types of acid–base disorders can be defined by the relationship between the three variables, pH, Pco2, and HCO3 –. Respiratory disturbances begin with an increase or decrease in pulmonary carbon dioxide clearance which—through a shift in the equilibrium between CO2, H2O, and HCO3 –—favours a decreased hydrogen ion concentration (respiratory alkalosis) or an increased hydrogen ion concentration (respiratory acidosis) respectively. Metabolic acidosis may result when hydrogen ions are added with a nonbicarbonate anion, A−, in the form of HA, in which case bicarbonate is consumed, or when bicarbonate is removed as the sodium or potassium salt, increasing hydrogen ion concentration. Metabolic alkalosis is caused by removal of hydrogen ions or addition of bicarbonate. Laboratory tests usually performed in pursuit of diagnosis, aside from arterial blood gas analysis, include a basic metabolic profile with electrolytes (sodium, potassium, chloride, bicarbonate), blood urea nitrogen, and creatinine. Calculation of the serum anion gap, which is determined by subtracting the sum of chloride and bicarbonate from the serum sodium concentration, is useful. The normal value is 10 to 12 mEq/litre. An elevated value is diagnostic of metabolic acidosis, helpful in the differential diagnosis of the specific metabolic acidosis, and useful in determining the presence of a mixed metabolic disturbance. Acid–base disorders can be associated with (1) transport processes across epithelial cells lining transcellular spaces in the kidney, gastrointestinal tract, and skin; (2) transport of acid anions from intracellular to extracellular spaces—anion gap acidosis; and (3) intake.

Transepithelial ammonia concentration gradients in inner medulla of the rat

1987 ◽  
Vol 252 (3) ◽  
pp. F491-F500 ◽  
Author(s):  
D. W. Good ◽  
C. R. Caflisch ◽  
T. D. DuBose
Keyword(s):  
Metabolic Acidosis ◽  
Collecting Duct ◽  
Ammonia Concentration ◽  
Loop Of Henle ◽  
Concentration Gradients ◽  
Chronic Metabolic Acidosis ◽  
Inner Medullary Collecting Duct ◽  
Vasa Recta ◽  
Collecting Ducts ◽  
Medullary Collecting Duct

Transport of NH3 from loops of Henle to medullary collecting ducts has been proposed to play an important role in renal ammonia excretion. To determine whether transepithelial ammonia concentration gradients capable of driving this transport are present in the inner medulla, micropuncture experiments were performed in control rats and in rats with chronic metabolic acidosis. In situ pH and total ammonia concentrations were measured to calculate NH3 concentrations ([NH3]) for base and tip collecting duct, loop of Henle, and vasa recta. In control and acidotic rats, [NH3] in the loop of Henle was significantly greater than [NH3] in the collecting ducts. [NH3] did not differ in loop of Henle and adjacent vasa recta in either group of rats, indicating that NH3 concentration gradients between loop and collecting duct represent NH3 gradients that are present between medullary interstitium and collecting duct. During acidosis, an increase in collecting duct ammonia secretion was associated with an increase in the NH3 concentration difference between loop of Henle and collecting duct but occurred in the absence of a fall in collecting duct pH. The NH3 concentration gradient favoring diffusion of NH3 into the collecting ducts increased during acidosis because [NH3] in the loop of Henle and medullary interstitium increased more than [NH3] in the collecting duct. These findings indicate that transport processes involved in medullary ammonia accumulation play an important role in regulating ammonia secretion into the inner medullary collecting duct in vivo and that a fall in inner medullary collecting duct pH is not necessarily required for ammonia secretion by this segment to increase during chronic metabolic acidosis.

scholarly journals Hyperchloremic metabolic acidosis during bipolar transurethral resection of the prostate: a report of two cases

2021 ◽  
Vol 49 (6) ◽  
pp. 030006052110244
Author(s):  
Ann Hee You ◽  
Ji Yoo Lee ◽  
Jeong-Hyun Choi ◽  
Mi Kyeong Kim
Keyword(s):  
Metabolic Acidosis ◽  
Transurethral Resection ◽  
Normal Saline ◽  
Isotonic Saline ◽  
Hemodynamic Instability ◽  
Acid Base ◽  
Electrolyte Disturbance ◽  
Irrigation Fluid ◽  
Laboratory Test Results ◽  
Hyperchloremic Metabolic Acidosis

Compared with monopolar transurethral resection of the prostate (TURP), which requires electrolyte-free irrigation fluid, normal saline can be used as the irrigation solution in bipolar and laser TURP. The risk of TURP syndrome and severe electrolyte disturbance is minimized when normal saline is used as the irrigation fluid. However, the use of isotonic saline also causes acid-base imbalance and electrolyte disturbance. We experienced two patients who developed hyperchloremic metabolic acidosis during bipolar TURP. After proper intervention, hemodynamic instability resolved, and laboratory test results normalized. Anesthesiologists must pay attention to acid-base and electrolyte status when rapid absorption of excessive isotonic solution is suspected, even during bipolar and laser TURP, which use normal saline as the irrigation fluid.

scholarly journals Ion Transport and the Development of Hydrogen Ion Secretion in the Stomach of the Metamorphosing Bullfrog Tadpole

1969 ◽  
Vol 54 (1) ◽  
pp. 76-95 ◽  
Author(s):  
John G. Forte ◽  
Liangchai Limlomwongse ◽  
Dinkar K. Kasbekar
Keyword(s):  
Ion Transport ◽  
Active Transport ◽  
Hydrogen Ion ◽  
Equilibrium Potential ◽  
Flux Analysis ◽  
Cell Interior ◽  
Ion Secretion ◽  
Hcl Secretion ◽  
Bullfrog Tadpole ◽  
Induced Changes

Isolated bullfrog tadpole stomachs secrete H+ by stage XXIV of metamorphosis, when tail reabsorption is nearly complete. At this stage the PD shows characteristic responses identical to those of the adult. The appearance of HCl secretion correlates well with other studies showing the morphogenesis of oxyntic cells. Prior to the development of H+ secretion tadpole stomachs maintain a PD similar in polarity and magnitude to that of the adult; i.e., secretory (S) side negative with respect to the nutrient (N) side. The interdependence with aerobic metabolism appeared to increase progressively through metamorphosis; however, glycolytic inhibitors always abolished the PD. Isotopic flux analysis showed that the transepithelial movement of Na+ was consistent with passive diffusion, whereas an active transport of Cl- from N to S was clearly indicated. Variations in [Na+], [K+], and [Cl-] in the bathing solutions induced changes consistent with the following functional description of the pre-H+-secreting tadpole stomach. (a) The S side is relatively permeable to Cl-, but not to Na+ or K+. (b) An equilibrium potential for K+ and Cl- exists at the N interface. (c) Ouabain abolishes the selective K+ permeablity at the N interface and reduces the total PD. (d) Effects of Na+ replacement by choline in the N solution become manifest only below 10–20 mM. It is concluded that prior to development of H+ secretion, the tadpole gastric PD is generated by a Cl- pump from N to S and a Na+ pump operating from the cell interior toward the N side.

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