CERTAIN ASPECTS OF THE RENAL REGULATION OF BODY COMPOSITION

PEDIATRICS ◽  
1954 ◽  
Vol 14 (6) ◽  
pp. 567-572
Author(s):  
ROBERT E. COOKE
Keyword(s):  
Carbon Dioxide ◽  
Extracellular Space ◽  
Carbonic Acid ◽  
Plasma Concentrations ◽  
Extracellular Volume ◽  
Extracellular Fluid ◽  
Carbon Dioxide Tension ◽  
Plasma Sodium ◽  
Renal Tubules ◽  
Bicarbonate Concentration

THE pH of extracellular fluid is determined by the ratio of the plasma concentrations of bicarbonate ion to carbonic acid, as given in the classical Henderson-Hasselbach equation. [See Equation in Source Pdf] The denominator the carbonic acid concentration, [H2CO3], is proportional to the carbon dioxide tension of the blood. The carbon dioxide tension (pCO2) is primarily dependent upon respiratory function, since metabolism (hence carbon dioxide production) is relatively constant. The numerator of the equation—the bicarbonate concentration of extracellular fluid—is determined by the difference between nonvolatile cations and anions. Since there are almost limitless quantities of bicarbonate available to the organism from cell metabolism, [See Equation in Source Pdf] bicarbonate concentration must change whenever nonvolatile cation (largely sodium) is altered in relation to nonvolatile anion (largely chloride). Thus in most states extracellular bicarbonate concentration is dependent upon the ratio of sodium to chloride in extracellular fluid. The quantity of water filtered at the glomeruli and reabsorbed by the renal tubules each day is approximately 15 times the extracellular volume. The quantity of sodium chloride filtered and reabsorbed daily is approximately 15 times that contained in the extracellular space and 150 times that usually ingested and excreted each day. Therefore, the ratio of plasma sodium to chloride in any steady state is determined by the composition of the renal tubular reabsorbate, as Cushny pointed over 30 years ago. In a sense the kidney perfuses the extracellular space with large quantities of tubular reabsorbate. Tubular reasorbate—the net quantity of materials reabsorbed by the tubules. This term is analogous to glomerular filtrate—the quantity of materials filtered by the glomeruli.

The Antidiuretic Effect of Chronic Hydrochlorothiazide Treatment in Rats with Diabetes Insipidus: Water and Electrolyte Balance

1982 ◽  
Vol 63 (6) ◽  
pp. 525-532 ◽  
Author(s):  
S. J. Walter ◽  
J. Skinner ◽  
J. F. Laycock ◽  
D. G. Shirley
Keyword(s):  
Diabetes Insipidus ◽  
Extracellular Volume ◽  
Urine Volume ◽  
Extracellular Fluid ◽  
Urinary Sodium Excretion ◽  
Sodium Concentration ◽  
Sodium Balance ◽  
Plasma Sodium ◽  
Electrolyte Balance ◽  
Antidiuretic Effect

1. The antidiuretic effect of hydrochlorothiazide in diabetes insipidus was investigated in rats with the hereditary hypothalamic form of the disease (Brattleboro rats). 2. Administration of hydrochlorothiazide in the food resulted in a marked fall in urine volume and a corresponding rise in osmolality. These effects persisted throughout the period of treatment (6–7 days). 3. Body weight and extracellular volume were significantly reduced in the thiazide-treated rats. 4. Hydrochlorothiazide caused an increase in urinary sodium excretion only on the first day of treatment. The resulting small negative sodium balance (in comparison with untreated rats) remained statistically significant for 2 days only. Thiazide-treated rats gradually developed a potassium deficit which was statistically significant from the fourth day of treatment. 5. Total exchangeable sodium, measured after 7 days of thiazide treatment, was not significantly different from that of untreated rats. However, plasma sodium was reduced in thiazide-treated animals, whereas erythrocyte sodium concentration was elevated. 6. It is concluded that the antidiuresis resulting from chronic hydrochlorothiazide administration is associated with a reduction in extracellular volume, but not with a significant overall sodium deficit. Hydrochlorothiazide appears to cause a redistribution of the body's sodium such that the amount of sodium in the extracellular fluid compartment is reduced.

Development of indices for determining extracellular fluid sodium and water status in acute diabetic ketoacidosis: possible tools for clinical audit

1994 ◽  
Vol 40 (5) ◽  
pp. 758-762
Author(s):  
D F Davidson ◽  
J Williamson ◽  
D E Boag ◽  
T Millar
Keyword(s):  
Diabetic Ketoacidosis ◽  
Water Status ◽  
Plasma Concentrations ◽  
Extracellular Fluid ◽  
Sodium Concentration ◽  
Hydration Status ◽  
Plasma Sodium ◽  
Plasma Sodium Concentration ◽  
Acute Diabetes ◽  
Extracellular Environment

Abstract The limitation of plasma sodium concentration as an indicator of extracellular hydration status in cases of acute diabetes is well recognized and could lead to individually inappropriate fluid therapy. However, in view of the small analytical and biological variations exhibited by plasma concentrations of protein, water, and sodium in health, we have developed simple laboratory indices that may better describe the extracellular environment. Preliminary data presented here for 20 patients with acute diabetic ketoacidosis admitted as emergencies to Crosshouse Hospital suggest that the type of approach we describe has the potential to supply meaningful therapeutic data to the managing physician and, therefore, merits further study in a clinical setting.

Buffer systems in the rumen of sheep. I. pH and bicarbonate concentration in relationship to pCO2.

1955 ◽  
Vol 6 (1) ◽  
pp. 115 ◽  
Author(s):  
AW Turner ◽  
VE Hodgetts
Keyword(s):  
Carbon Dioxide ◽  
Carbonic Acid ◽  
High Pco2 ◽  
Bicarbonate Concentration ◽  
Bulk Fluid ◽  
Ruminal Fluid ◽  
Arterial Blood ◽  
Wide Range ◽  
The Relationship ◽  
Hasselbalch Equation

Experiments are described which emphasize the importance of avoiding loss of carbon dioxide when estimating the pH or bicarbonate concentration of ruminal fluid. The high pCO2 of ruminal fluid is stressed; this may be 10 times or more as great as that of arterial blood. The relationship between pCO2, pH, and [HCO3-] was examined in terms of the Henderson-Hasselbalch equation over a wide range of pCO2. From this, the pK1' of the carbonic acid system in four ruminal fluids was determined as 6.21-6.28, mean 6.25. The higher pH of saliva-free samples of ruminal fluid withdrawn by suction through a tube passed down the oesophagus, as compared with that of the bulk fluid obtained through a ruminal fistula, is considered to be due to loss of carbon dioxide during collection. A better estimate of intraruminal pH is obtained, even when salivary contamination occurs, if such samples are equilibrated with a sample of the animal's ruminal gas; if this is not practicable, an arbitrary gas mixture of high pCO2, e.g. 50 per cent. carbon dioxide and nitrogen, may be used.

Acid-Base Changes in Brain and Blood of Rats Exposed to High Concentrations of Carbon Dioxide

1957 ◽  
Vol 192 (1) ◽  
pp. 91-94 ◽  
Author(s):  
David A. Brodie ◽  
Dixon M. Woodbury
Keyword(s):  
Carbonic Acid ◽  
Plasma Concentrations ◽  
Ion Concentration ◽  
Brain Cells ◽  
Bicarbonate Concentration ◽  
Abrupt Withdrawal ◽  
Blood Ph ◽  
Total Brain ◽  
High Concentrations ◽  
The Brain

Blood ph, total plasma CO2 and total brain CO2 were determined in the following groups of rats: untreated controls, exposure to 30% CO2, exposure to 50% CO2 and 30 seconds after abrupt withdrawal from 50% CO2. Values were calculated for plasma concentrations of bicarbonate ion and carbonic acid, and for intracellular brain CO2, carbonic acid, bicarbonate and ph. Inhalation of 30% CO2 increased carbonic acid and bicarbonate concentration in plasma and brain cells, and decreased intracellular ph moderately. When the concentration of inhaled CO2 was increased from 30 to 50%, there was a further marked fall in the ph of blood and brain cells, a significant further increase in the amount of carbonic acid in plasma and brain, but no significant further increase in the bicarbonate ion concentration in plasma or brain. On abrupt withdrawal of rats from 50% CO2, the ph of the blood and the brain moved into the range of the ph of the 30% CO2 rats, bicarbonate ion concentration fell below control values; brain bicarbonate ion concentration, however, remained markedly elevated.

scholarly journals A redefinition of normal acid-base equilibrium in man: Carbon dioxide tension as a key determinant of normal plasma bicarbonate concentration

1979 ◽  
Vol 16 (5) ◽  
pp. 612-618 ◽  
Author(s):  
Nicolaos E. Madias ◽  
Horacio J. Adrogué ◽  
Gary L. Horowitz ◽  
Jordan J. Cohen ◽  
William B. Schwartz
Keyword(s):  
Carbon Dioxide ◽  
Carbon Dioxide Tension ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Plasma Bicarbonate ◽  
Base Equilibrium ◽  
Normal Plasma ◽  
Acid Base Equilibrium ◽  
Normal Acid

Ionic transport mechanisms underlying fluid secretion by the pancreas

1981 ◽  
Vol 296 (1080) ◽  
pp. 167-178 ◽  
Keyword(s):  
Carbonic Acid ◽  
Basolateral Membrane ◽  
Extracellular Fluid ◽  
Fluid Secretion ◽  
Bicarbonate Concentration ◽  
Cellular Mechanisms ◽  
Luminal Membrane ◽  
Sodium Gradient ◽  
Characteristic Features ◽  
Sodium And Potassium

The pancreas is a ‘leaky’ epithelium and secretes a juice in which sodium and potassium have concentrations similar to those of plasma. The characteristic features of the secretion are its isosmolality and its high bicarbonate concentration. It is the latter that has attracted considerable attention. Secretion in the isolated cat pancreas is directly proportional to the bicarbonate concentration in the nutrient fluid. The ability of the gland to secrete weak acids has led to the view that because of the very different chemical nature of the anions, it is most likely that it is a component common to all buffers, the proton, that is subject to active transport. This is supported by the decrease in pH and the increase in p co 2 of the venous effluent when secretion occurs and the sensitivity of secretion to the pH of the nutritional extracellular fluid. It is proposed that the cellular mechanisms are as follows: CO 2 diffuses into the cell and is hydrated to carbonic acid under the influence of carbonic anhydrase. The bicarbonate ion so formed diffuses into the ductular lumen and the proton is transported backwards through the epithelium with a proton pump (Mg 2+ -ATPase) provisionally located in the luminal membrane and a hydrogen-sodium exchange carrier located in the basolateral membrane. Energy for the latter process is derived from the sodium gradient between extracellular fluid and cell. This gradient is maintained by a (Na + +K + )-ATPase also located in the basolateral membrane. Chloride appears to be transported partly through a chloride-bicarbonate exchange mechanism, but largely passively together with a large sodium and potassium com ponent through the paracellular pathway. Osmotic equilibrium is likely to occur in the small ductules.

Skeletal carbon dioxide stores during metabolic acidosis

1984 ◽  
Vol 247 (2) ◽  
pp. F326-F330 ◽  
Author(s):  
J. A. Bettice
Keyword(s):  
Carbon Dioxide ◽  
Metabolic Acidosis ◽  
Diabetic Ketoacidosis ◽  
Carbon Dioxide Tension ◽  
Carbon Dioxide Content ◽  
Chemical Induction ◽  
Bicarbonate Concentration ◽  
Blood Ph ◽  
Exchangeable Fraction

These experiments were performed to examine the buffering functions of skeletal carbon dioxide during metabolic acidosis. Acidosis of several days duration was produced in rats either by inclusion of acidogenic substances in the diet or by chemical induction of diabetic ketoacidosis. Titrimetric methods were used to measure the carbon dioxide content of bone, which was divided into readily exchangeable and slowly exchangeable pools according to a model described in the text. Acid feeding resulted in a mild acidemia (blood pH greater than 7.25), whereas profound metabolic acidemia occurred during diabetic ketoacidosis (blood pH less than 7.00). Total bone carbon dioxide was reduced during both forms of metabolic acidosis. This reduction in skeletal carbon dioxide occurred within the first 24 h after the onset of metabolic acidosis, was associated with a decline in the readily exchangeable fraction of skeletal carbon dioxide, and was directly proportional to the declines in extracellular bicarbonate concentration and plasma carbon dioxide tension.

Effects of Intravenous Infusion of Carbonic Anhydrase on Carbon Dioxide Tension of Alkaline Urine

1956 ◽  
Vol 185 (2) ◽  
pp. 426-429 ◽  
Author(s):  
Bruno K. Ochwadt ◽  
Robert F. Pitts
Keyword(s):  
Carbon Dioxide ◽  
Carbonic Anhydrase ◽  
Sodium Bicarbonate ◽  
Renal Tubule ◽  
Carbonic Acid ◽  
Carbon Dioxide Tension ◽  
High Carbon ◽  
Priming Dose ◽  
Alkaline Urine ◽  
High Carbon Dioxide

Five dogs were rendered hydropenic by withholding water for 20 hours and mildly alkalotic by the infusion of sodium bicarbonate intravenously in small amounts. Under these conditions alkaline urine was formed at approximately 1.0 cc/min. In 15 control periods the pCO2 of the urine exceeded that of the plasma, the ratio averaged 2.08 ± 0.44 (S.D.) with a range of 1.45–2.79. Following the intravenous administration of 100 mg of carbonic anhydrase as a priming dose and the infusion of the enzyme at a rate of 1 mg/min., the ratio in 25 experimental periods decreased to an average of 0.988 ± 0.14 (S.D.) with a range of 0.78–1.30. We conclude that the high carbon dioxide tensions commonly observed in alkaline urines result from delayed dehydration of carbonic acid to carbon dioxide in the renal tubule.

Sign in / Sign up

Export Citation Format

Share Document