Chloride Titration in the Dog: The Influence of Extracellular Fluid Expansion on the Pattern of Chloride Reabsorption

1973 ◽  
Vol 44 (4) ◽  
pp. 385-395 ◽  
Author(s):  
J. J. Cohen ◽  
Y. Bar-Khayim ◽  
S. Garella ◽  
J. A. Chazan
Keyword(s):  
Wide Spectrum ◽  
Extracellular Fluid ◽  
Chloride Concentration ◽  
Specific Pattern ◽  
Sodium Reabsorption ◽  
Elevated Plasma ◽  
Chloride Homeostasis ◽  
Threshold Mechanism ◽  
Two Factors ◽  
Plasma Chloride

1. The technique of chloride titration was employed in twenty dogs to determine the pattern of renal chloride handling in response to systematic increases in filtered chloride load. The influence of variations in sodium reabsorption on this pattern was also assessed by producing a wide spectrum of volume expansion during the titration protocols. 2. The results indicate that chloride reabsorption is proportional both to the rate of chloride filtration and to the rate of sodium reabsorption and, hence, that the specific pattern of each chloride titration curve is the fortuitous consequence of the interplay between these two factors. 3. The rate of chloride reabsorption relative to the simultaneous rate of sodium reabsorption was used as an index of the ability of the kidney to maintain chloride homeostasis and indicated that the kidney invariably tends to return depressed. plasma chloride concentration towards normal but, under the conditions of these acute experiments, consistently tends to reduce elevated plasma chloride concentration only when cation reabsorption is markedly depressed. 4. The present observations do not elucidate the mechanism responsible for these findings but suggest that plasma chloride concentration is not regulated through the operation of a threshold mechanism.

Chloride concentration gradient in newborn dogs in the presence of distal nephron blockade

1980 ◽  
Vol 239 (4) ◽  
pp. F328-F335
Author(s):  
Aviad Haramati ◽  
Leonard I. Kleinman
Keyword(s):  
Proximal Tubule ◽  
Ethacrynic Acid ◽  
Chloride Concentration ◽  
Sodium Reabsorption ◽  
Distal Nephron ◽  
Electrolyte Excretion ◽  
Newborn Animal ◽  
Plasma Chloride ◽  
Renal Tubular ◽  
Inner Cortex

Renal tubular Na+, Cl-, and H2O reabsorption was determined in 14 newborn dogs, 3–29 days of age, and in three adult dogs. In all animals NaCl reabsorption beyond the proximal tubule was blocked with ethacrynic acid (2 mg/kg) and amiloride (2.4 mg/kg). During distal blockade, fractional reabsorption of NaCl and water in both newborns and adults was approximately 70%, and there was a urine-to-plasma chloride gradient equal to 1.34 ± 0.01, indicating that the proximal tubules of the newborn as well as those of the adult can generate a transtubular Cl- gradient. Upon administration of acetazolamide (50 mg/kg), there was a dramatic increase in excretion of Na+, Cl-, HCO3-, and water, and a decrease in the transtubular chloride gradient. After acetazolamide, the degree of inhibition of HCO3- reabsorption was well correlated with that of Na+ (r = 0.77) or Cl- (r = 0.74), and Na+ or Cl- inhibition exceeded that of HCO3- In the newborn animal, the ratio of inner-to-outer cortical nephron function is high at birth and declines rapidly during the first few weeks of life. However, there was no correlation between age and changes in either electrolyte excretion or in the transtubular chloride gradient. Therefore, the newborn dog possesses Cl- permselective tubules in the inner cortex that, in the presence of intact HCO3- reabsorption, are capable of establishing a functional transtubular Cl- gradient contributing to NaCl reabsorption. bicarbonate reabsorption; sodium reabsorption; ethacrynic acid; amiloride; acetazolamide; proximal tubule Submitted on October 29, 1979 Accepted on April 18, 1980

Hyponatremia in the rat in the absence of positive water balance.

1997 ◽  
Vol 8 (4) ◽  
pp. 524-529
Author(s):  
M Gowrishankar ◽  
C B Chen ◽  
S Cheema-Dhadli ◽  
A Steele ◽  
M L Halperin
Keyword(s):  
Water Balance ◽  
Isotonic Saline ◽  
Extracellular Fluid ◽  
Free Water ◽  
Control Group ◽  
High Concentration ◽  
Additional Control ◽  
Two Factors ◽  
Negative Balance ◽  
Usual Diet

The purpose of this report is to determine the mechanisms that lead to hyponatremia when isotonic saline was the only fluid infused into rats given antidiuretic hormone (ADH), and what might minimize the degree of this hyponatremia. Normal rats were deprived of food and water for the 24-hr study period. They received an infusion of isotonic saline to expand their extracellular fluid (ECF) volume with and without exogenous ADH administration (N = 8 in each of the four groups). Similar studies were also carried out in 32 rats fed a low electrolyte diet for 72 hr before the experiment. An additional control group was fed the low electrolyte diet supplemented with sodium (Na), potassium (K), and chloride (Cl). Hyponatremia developed over 24 hr in rats fed their usual diet if treated with ADH and isotonic saline (fall, 13 +/- 2 mM, P < 0.01). The hyponatremia was caused by negative balance for Na + K salts. Hyponatremia did not develop after the saline + ADH treatment if rats were pretreated for 3 days with a low electrolyte diet. Two factors were required to develop this hyponatremia--generation of electrolyte-free water as a result of the excretion of a large quantity of Na + K salts at a high concentration in the urine, and prevention of the excretion of this electrolyte-free water by ADH. Increasing the avidity for Na reabsorption by the kidney prevented this type of hyponatremia from developing.

Renal sodium handling in normal humans subjected to low, normal, and extremely high sodium supplies

1985 ◽  
Vol 249 (6) ◽  
pp. F941-F947 ◽  
Author(s):  
J. C. Roos ◽  
H. A. Koomans ◽  
E. J. Dorhout Mees ◽  
I. M. Delawi
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Sodium Intake ◽  
Extracellular Fluid ◽  
Plasma Renin ◽  
Renin Activity ◽  
Sodium Reabsorption ◽  
Lithium Clearance ◽  
Renal Sodium Handling ◽  
Sodium Handling

We studied renal sodium handling, extracellular fluid volume (ECFV), plasma renin activity, aldosterone and norepinephrine, and blood pressure in eight healthy volunteers after equilibration on intakes of 20, 200, and 1,128 +/- 141 meq sodium, respectively. Renal sodium handling was assessed by means of clearance studies during maximal water diuresis and lithium clearance. Urinary sodium excretions were 22 +/- 4, 202 +/- 19, and 1,052 +/- 86 meq/day. From the lower to the upper sodium intake level, 24-h creatinine clearance rose from 111 +/- 7 to 136 +/- 11 ml/min and inulin clearance from 103 +/- 9 to 129 +/- 9 ml/min, whereas proximal and distal fractional sodium reabsorption (FSRprox and FSRdist, respectively) fell from 86.8 +/- 1.3 to 79.0 +/- 2.7% and from 96.5 +/- 0.5 to 76.0 +/- 1.9%, respectively. During the normal sodium intake (200 meq), intermediate values were recorded. The changes in fractional lithium clearance were less consistent but correlated with FSRprox (r = 0.78, P less than 0.001) and not with FSRdist. Major changes in plasma renin activity, aldosterone, and, to a lesser extent, norepinephrine accompanied these changes in kidney function, displaying inverse and exponential correlations with daily sodium excretion and ECFV. No consistent rise in blood pressure was detected. These observations indicate that in healthy humans renal adaptation to vast variations in sodium intake includes resetting of glomerular filtration rate, FSRprox, and, in particular, FSRdist. Alterations in neurohumoral factors may play a dominant role in this adaptation.

Quantitative relationship of renal glucose and sodium reabsorption during ECF expansion

1975 ◽  
Vol 229 (1) ◽  
pp. 66-71 ◽  
Author(s):  
Higgins JT ◽  
AE Meinders
Keyword(s):  
Proximal Tubule ◽  
Isotonic Saline ◽  
Extracellular Fluid ◽  
Quantitative Relationship ◽  
Ringer Solution ◽  
Sodium Balance ◽  
Sodium Reabsorption ◽  
Coupled Transport ◽  
Appearance Time ◽  
Glucose Reabsorption

To investigate the quantitative relationship between glucose and sodium reabsorption during extracellular fluid (ECF) expansion and to examine the possible contribution to glucosuria of passive diffusion of glucose from peritubular blood to tubular fluid, renal clearance studies were carried out in dogs. It was found that ECF expansion with isotonic saline or Ringer solution causes a decrease in the maximal rate of glucose reabsorption (TmGlc), which is inversely and linearly related to fractional sodium excretion (FENa) over a range from less than 1% more than 25% FENa (r equals -0.394, P less than 0.001). A continuous relationship between TmGlc and FENa could be demonstrated as the ECF was expanded in individual animals as well as in pooled data. Infusion of albumin solution to preferentially expand the plasma volume and decrease proximal tubular sodium reabsorption produced a 24% fall in TmGlc suggesting that the proximal tubule is the site of interrelated glucose and sodium reabsorption. After pulse injections into the renal artery, [14-C]glucose and insulin had the same appearance time in the urine, thus failing to demonstrate diffusion of glucose from blood into the tubule in saline-loaded dogs as well as in dogs in normal sodium balance. It is suggested that ECF expansion exerts its effect on glucose reabsorption by inhibiting the coupled transport of glucose and sodium across the epithelium of the renal proximal tubule.

Influence of Hydrostatic and Oncotic Pressure on Sodium Reabsorption in the Unilateral Pyelonephritic Dog Kidney

1974 ◽  
Vol 47 (4) ◽  
pp. 367-376
Author(s):  
J. P. Wagnild ◽  
F. D. Gutmann ◽  
R. E. Rieselbach
Keyword(s):  
Sodium Chloride ◽  
Volume Expansion ◽  
Extracellular Fluid ◽  
Sodium Reabsorption ◽  
Oncotic Pressure ◽  
Peritubular Capillary ◽  
Physical Force ◽  
Dog Kidney ◽  
Capillary Fluid ◽  
Diseased Kidney

1. The diseased kidney in the dog with experimental unilateral reduction in nephron population, has been shown previously to undergo an exaggerated inhibition of sodium reabsorption after extracellular fluid (ECF) volume expansion induced by isotonic sodium chloride solution compared with the control kidney. The latter serves to maintain a non-azotaemic environment. 2. In the present studies, manoeuvres designed to alter predominantly either post-glomerular hydrostatic pressure (PGHP) or peritubular capillary oncotic pressure (COP) were performed to investigate further the mechanism of this exaggerated natriuresis. 3. Volume expansion with 5 g/dl albumin in 145 mmol/l sodium chloride (saline), thereby increasing PGHP without changing COP, produced exaggerated diseased kidney natriuresis, but of a smaller magnitude than when the same dogs were studied under a lesser degree of intravascular volume expansion with 145 mmol/l saline. Renal vasodilatation produced by systemically administered dopamine, which increases PGHP without ECF volume expansion, also produced exaggerated natriuresis by the diseased kidney. 4. A selective decrease in COP induced by expansion with saline in conjunction with trimethophan camsylate (Arfonad)-induced hypotension also produced exaggerated diseased kidney natriuresis, but to a lesser degree than saline expansion alone in the same dogs. 5. Thus experimental manoeuvres designed to reduce peritubular capillary fluid reabsorption by either predominantly increasing PGHP or decreasing COP produced exaggerated diseased kidney natriuresis. This exaggerated natriuretic response to manoeuvres which predominantly altered either physical force by itself did not approach the response elicited by expansion with saline. 6. The data suggest that alterations in Starling forces play an important role in mediating the exaggerated diseased kidney natriuresis after an acute saline load.

Studies on Mineralocorticoid ‘Escape’ in Cirrhosis

1979 ◽  
Vol 56 (5) ◽  
pp. 401-406 ◽  
Author(s):  
S. P. Wilkinson ◽  
I. K. Smith ◽  
Helen Moodie ◽  
Lucilla Poston ◽  
R. Williams
Keyword(s):  
Extracellular Fluid ◽  
Plasma Renin ◽  
Fluid Volume ◽  
The Other ◽  
Extracellular Fluid Volume ◽  
Sodium Reabsorption ◽  
Sodium Retention ◽  
Similar Extent ◽  
Water Diuresis ◽  
Diluting Segment

1. The mineralocorticoid 9α-fluorohydrocortisone was given to 12 patients with cirrhosis without ascites. In seven an ‘escape’ from its sodium-retaining effects was observed, the other five continuing to retain sodium. 2. Changes in plasma renin activity (PRA) and inulin clearance (Cinulin) were used in the assessment of possible changes in the ‘effective’ extracellular fluid volume. PRA fell and Cinulin increased to a similar extent in each of the two groups of patients. These findings do not support the concept that the failure to show the mineralocorticoid escape in some patients with cirrhosis is due to a failure of expansion of the effective extracellular fluid volume. 3. Sodium reabsorption in the different segments of the nephron as estimated by clearance techniques under conditions of maximal water diuresis showed that the greatest changes to account for both mineralocorticoid escape and sodium retention were in the part of the nephron beyond the diluting segment.

Adenovirus-mediated human prostasin gene delivery is linked to increased aldosterone production and hypertension in rats

2003 ◽  
Vol 284 (4) ◽  
pp. R1031-R1036 ◽  
Author(s):  
Cindy Wang ◽  
Julie Chao ◽  
Lee Chao
Keyword(s):  
Blood Pressure ◽  
Gene Transfer ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Sodium Reabsorption ◽  
Elevated Plasma ◽  
Aldosterone Production ◽  
Renal Kallikrein

Prostasin has been demonstrated to be an activator of epithelial sodium channels in cultured renal and bronchial epithelial cells. In this study, we evaluated the effects of adenovirus-mediated gene transfer of human prostasin on blood pressure regulation and sodium reabsorption in Wistar rats. Expression of human prostasin mRNA was identified in rat adrenal gland, liver, kidney, heart, lung, and aorta, and immunoreactive human prostasin was detected in the circulation and urine of rats receiving prostasin gene transfer. A single injection of adenovirus carrying the prostasin gene caused prolonged increases in blood pressure for 3–4 wk. Blood pressure increase was accompanied by elevated plasma aldosterone levels and reduced plasma renin activity. The increase in blood pressure and plasma aldosterone levels as well as the reduction of plasma renin activity correlated with the expression of human prostasin transgene. Elevated plasma aldosterone levels were detected at 3 days after gene transfer before the development of hypertension, indicating that stimulation of mineralocorticoid production is the primary target of prostasin. Prostasin gene transfer significantly reduced urinary K+ excretion but increased urinary Na+ and kallikrein excretion. Elevated renal kallikrein levels promote natriuresis, which may lead to sodium escape and prevent further increases of blood pressure after prostasin gene transfer. In summary, these results suggest that prostasin participates in blood pressure and electrolyte homeostasis by regulating the renin-angiotensin-aldosterone and kallikrein-kinin systems.

FURTHER OBSERVATIONS ON METABOLIC ALTERATIONS IN THE HYPOTHERMIC RAT

1961 ◽  
Vol 39 (1) ◽  
pp. 1-8 ◽  
Author(s):  
John R. Beaton
Keyword(s):  
Water Content ◽  
Chloride Concentration ◽  
Plasma Potassium ◽  
Inorganic Phosphorus ◽  
Plasma Sodium ◽  
Red Cell ◽  
Metabolic Alterations ◽  
Plasma Chloride ◽  
Sodium And Potassium ◽  
Sodium Plasma

Further observations on metabolic alterations in fasted rats cooled under ice to rectal temperatures approximating 15 °C are reported. In the hypothermic rats, metabolism of injected lactic acid does not appear to be impaired. There is however: increased concentration of inorganic phosphorus in blood but not in liver; increased concentration of glutathione in liver but not in blood; increased plasma chloride concentration; decreased red cell potassium concentration; increased red cell water content; decreased plasma water content. Hypothermia, under these conditions, did not alter concentrations of liver acid-extractable glycogen, red cell sodium, plasma sodium, plasma potassium, nor serum calcium. Administration of urea in saline prior to cooling elevated plasma sodium and potassium concentrations in hypothermic rats. These observations are discussed in relation to previously reported effects of hypothermia on carbohydrate metabolite levels.

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