Effect of Changes in the Volume of Extracellular Fluid on Sodium Reabsorption in the Proximal and Distal Tubule1

2015 ◽  
pp. 26-39
Author(s):  
J. P. Hayslett ◽  
M. Kashgarian ◽  
M. W. Weiner ◽  
F. H. Epstein
Keyword(s):  
Extracellular Fluid ◽  
Sodium Reabsorption

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.

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.

scholarly journals Epithelial Sodium Channel and Salt-Sensitive Hypertension

Hypertension ◽  
2021 ◽  
Vol 77 (3) ◽  
pp. 759-767
Author(s):  
Stephanie M. Mutchler ◽  
Annet Kirabo ◽  
Thomas R. Kleyman
Keyword(s):  
Blood Pressure ◽  
Sodium Channel ◽  
Salt Intake ◽  
Extracellular Fluid ◽  
Pressure Rise ◽  
Epithelial Sodium Channel ◽  
Sodium Reabsorption ◽  
High Salt Intake ◽  
Salt Sensitive Hypertension

The development of high blood pressure is influenced by genetic and environmental factors, with high salt intake being a known environmental contributor. Humans display a spectrum of sodium-sensitivity, with some individuals displaying a significant blood pressure rise in response to increased sodium intake while others experience almost no change. These differences are, in part, attributable to genetic variation in pathways involved in sodium handling and excretion. ENaC (epithelial sodium channel) is one of the key transporters responsible for the reabsorption of sodium in the distal nephron. This channel has an important role in the regulation of extracellular fluid volume and consequently blood pressure. Herein, we review the role of ENaC in the development of salt-sensitive hypertension, and present mechanistic insights into the regulation of ENaC activity and how it may accelerate sodium-induced damage and dysfunction. We discuss the traditional role of ENaC in renal sodium reabsorption and review work addressing ENaC expression and function in the brain, vasculature, and immune cells, and how this has expanded the implications for its role in the initiation and progression of salt-sensitive hypertension.

Possible Involvement of Up-regulated Salt Dependent Glucose Transporter-5 (SGLT5) in High-fructose Diet-induced Hypertension

2021 ◽  
Author(s):  
Hiroaki Hara ◽  
Kaori Takayanagi ◽  
Taisuke Shimizu ◽  
Takatsugu Iwashita ◽  
Akira Ikari ◽  
...  
Keyword(s):  
Glucose Transporter ◽  
Salt Intake ◽  
Extracellular Fluid ◽  
Sodium Reabsorption ◽  
High Fructose Diet ◽  
Fructose Metabolism ◽  
High Fructose ◽  
Induced Hypertension ◽  
Underlying Mechanisms ◽  
Salt Sensitive Hypertension

Abstract Excessive fructose intake causes a variety of adverse conditions (e.g., obesity, hepatic steatosis, insulin resistance and uric acid overproduction). Particularly, high fructose-induced hypertension is the most common and significant pathological setting, however, its underlying mechanisms are not established. We investigated these mechanisms in 7-week-old male SD rats fed a diet containing 60% glucose (GLU) or 60% fructose (FRU) for 3, 6, or 12 weeks. Daily food consumption was measured to avoid between-group discrepancies in caloric/salt intake, adjusting for feeding amounts. The FRU rats' mean blood pressure was significantly higher and fractional sodium excretion (FENa) was significantly lower, indicating that the high-fructose diet caused salt retention. The FRU rats' kidney weight and glomerular surface area were greater, suggesting that the high-fructose diet induced an increase in extracellular fluid volume. The GLUT5 and ketohexokinase expressions, an enzyme required for fructose metabolism, were up-regulated in FRU. Cortical ATP levels were significantly lower in FRU, which might indicate ATP consumption due to fructose metabolism. Unlike previous reports, the high-fructose diet did not affect NHE3 expression. A gene chip analysis conducted to identify susceptible molecules revealed that only Slc5a10 (corresponding to SGLT5) in FRU showed >2-fold up-regulation versus GLU. RT-PCR and in situ hybridization confirmed the SGLT5 up-regulation. Our findings may indicate that the high-fructose diet increased sodium reabsorption principally through up-regulated SGLT5, finally causing salt-sensitive hypertension.

Disorders of Water and Sodium Balance

2014 ◽  
Author(s):  
Richard H Sterns
Keyword(s):  
Water Conservation ◽  
Body Fluid ◽  
Cell Volume Regulation ◽  
Extracellular Fluid ◽  
Sodium Balance ◽  
Sodium Reabsorption ◽  
Renal Tubules ◽  
Response Curves ◽  
Volume Depletion ◽  
Fluid Compartment

Water accounts for approximately half of an adult human’s body weight. Two thirds of body water is intracellular, and the remaining one third is contained in the extracellular fluid compartment, which includes intravascular (plasma) and interstitial fluid. Small amounts of water are also contained in bone, dense connective tissue, digestive secretions, and cerebrospinal fluid. To maintain the stability of the internal milieu, body fluids are processed by the kidney, guided by intricate physiologic control systems that regulate fluid volume and composition. This chapter reviews the regulation of body fluid volumes, cell volume regulation in hypotonicity and hypertonicity, disorders of water excess (hyponatremia), water deficiency (hypernatremia), water conservation (diabetes insipidus), saltwater excess (edematous states), and saltwater deficiency (volume depletion). Tables describe control of body fluid volumes, causes of nonhypotonic hyponatremia, causes and treatment of acute hyponatremia, causes of the syndrome of inappropriate release of antidiuretic hormone (SIADH), and causes of hypernatremia. Figures illustrate sodium reabsorption by the renal tubules, the relationship between plasma vasopressin levels, renal sodium handling, and dose-response curves for a loop diuretic in patients with normal and reduced renal function. This chapter contains 4 highly rendered figures, 5 tables, 88 references, and 5 MCQs.

scholarly journals Role of the Kidneys in Resistant Hypertension

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Z. Khawaja ◽  
C. S. Wilcox
Keyword(s):  
Resistant Hypertension ◽  
Salt Intake ◽  
Antihypertensive Drugs ◽  
Critical Role ◽  
Diuretic Therapy ◽  
Extracellular Fluid ◽  
Treatment Resistance ◽  
Sodium Reabsorption ◽  
Dietary Salt ◽  
Dietary Salt Intake

Resistant hypertension is a failure to achieve goal BP (<140/90 mm Hg for the overall population and <130/80 mm Hg for those with diabetes mellitus or chronic kidney disease) in a patient who adheres to maximum tolerated doses of 3 antihypertensive drugs including a diuretic. The kidneys play a critical role in long-term regulation of blood pressure. Blunted pressure natriuresis, with resultant increase in extracellular fluid volume, is an important cause of resistant hypertension. Activation of the renin-angiotensin-aldosterone system, increased renal sympathetic nervous system activity and increased sodium reabsorption are important renal mechanisms. Successful treatment requires identification and reversal of lifestyle factors or drugs contributing to treatment resistance, diagnosis and appropriate treatment of secondary causes of hypertension, use of effective multidrug regimens and optimization of diuretic therapy. Since inappropriate renal salt retention underlies most cases of drug-resistant hypertension, the therapeutic focus should be on improving salt depleting therapy by assessing and, if necessary, reducing dietary salt intake, optimizing diuretic therapy, and adding a mineralocorticoid antagonist if there are no contraindications.

Aldosterone in the exaggerated natriuresis of spontaneously hypertensive rats

1978 ◽  
Vol 234 (1) ◽  
pp. F29-F35 ◽  
Author(s):  
L. R. Willis ◽  
J. H. Bauer
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Extracellular Fluid ◽  
Urinary Sodium Excretion ◽  
Sodium Reabsorption ◽  
Hypertensive Rats ◽  
Plasma Aldosterone Concentration ◽  
Salt Loading ◽  
Spontaneously Hypertensive ◽  
Salt Load ◽  
Total Body

The effect of mineralocorticoid hormones on the urinary responses of spontaneously hypertensive and normotensive rats to oral salt loading was determined. In response to a control salt load, the increase was determined. In response to a control salt load, the increase in urinary sodium excretion by the spontaneously hypertensive rats was significantly greater than that of the normotensive rats [48 +/- 6 (SE) mueq/h vs. 26 +/- 4 mueq/h]. Treatment with spironolactone did not significantly alter the natriuretic response of the spontaneously hypertensive rats (43 +/- 8 mueq/h) to another salt load, but increased the natriuretic response of the normotensive rats (55 +/- 7 mueq/h) to that of the hypertensive rats. D-Aldosterone suppressed the natriuretic response to salt loading of the hypertensive rats to a level which was not significantly different from that of the normotensive rats. Plasma aldosterone concentration was significantly lower in the spontaneously hypertensive rats than in the normotensive rats (18.0 +/- 3.3 and 52.1 +/- 5.2 ng/100 ml, respectively). Neither extracellular fluid volume nor total body water in spontaneously hypertensive and normotensive rats were significantly different. The data support the hypothesis that the exaggerated natriuresis in the spontaneously hypertensive rats is mediated by a relative lack by these rats of aldosterone-mediated distal tubular sodium reabsorption.

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