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.

Estimates of Extracellular Fluid Volume of Myocardium

1955 ◽  
Vol 184 (1) ◽  
pp. 171-174 ◽  
Author(s):  
William Van B. Robertson ◽  
Pincus Peyser
Keyword(s):  
Reference Material ◽  
Extracellular Fluid ◽  
Fluid Volume ◽  
The Other ◽  
Extracellular Fluid Volume

The extracellular fluid volume of the myocardium was determined in nephrectomized cats using sucrose as a reference material. This was allowed to equilibrate for one day before analysis. The chloride space, sodium space and an extracellular fluid volume based on the Conway-Boyle hypothesis were also determined. The sucrose space was smaller than, but bore no consistent relation to any of the other volumes. The sucrose space increased following an injection of epinephrine.

Influence of Volume Expansion on Renal Diluting Capacity in the Rat

1974 ◽  
Vol 46 (3) ◽  
pp. 331-345
Author(s):  
M. Martinez-Maldonado ◽  
G. Eknoyan ◽  
W. N. Suki
Keyword(s):  
Volume Expansion ◽  
Collecting Duct ◽  
Isotonic Saline ◽  
Extracellular Fluid ◽  
Free Water ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Sodium Reabsorption ◽  
Water Excretion ◽  
Hypotonic Saline

1. The functional capacity of Henle's loop was examined during hypotonic, isotonic and hypertonic extracellular fluid volume expansion. To eliminate a possible role of antidiuretic hormone (ADH) in the alteration of free water excretion, rats with congenital diabetes insipidus were used. The infusion of hypotonic saline resulted in a progressive rise in free water clearance (CH2O) throughout the range of urine flow (V) attained. Similar results were obtained in rats treated chronically with deoxycorticosterone acetate (DOCA). The infusion of isotonic saline (sodium chloride, 154 mmol/l) produced an initial rise in CH2O until V represented 10% of the filtered load, after which CH2O appeared to reach a plateau. The limitation of CH2O was more marked when hypertonic saline was infused. Medullary and papillary non-urea solute (NUS) concentration rose progressively with the increasing concentration of the saline solution infused. 2. The greater fractional sodium excretion (FENa) after acute isotonic and hypertonic volume expansion is probably the result of inhibition of sodium reabsorption in the collecting duct, although inhibition in the ascending limb cannot be entirely excluded. The depression of CH2O as a function of V seen during acute isotonic or hypertonic volume expansion can be attributed in part to enhanced water back-diffusion from the collecting duct consequent to the increasing medullary and papillary interstitial NUS concentration, even in the absence of ADH. 3. Chronic expansion of extracellular fluid volume by DOCA administration did not modify the response to hypotonic saline infusion.

Plasma Renin Activity, Plasma Angiotensin II and Extracellular Fluid Volume in Patients after Renal Transplantation

1976 ◽  
Vol 51 (s3) ◽  
pp. 227s-230s ◽  
Author(s):  
J. S. Horvath ◽  
C. Baxter ◽  
F. Furby ◽  
V. Hood ◽  
J. Johnson ◽  
...  
Keyword(s):  
Renal Transplantation ◽  
Sodium Intake ◽  
Extracellular Fluid ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Plasma Angiotensin

1. Patients with cadaveric renal transplants and plasma creatinine less than 177 μmol/l who had their own kidneys removed were studied. 2. The renin—angiotensin system appeared to behave in a normal fashion in response to alterations in sodium intake and posture. 3. The renin—angiotensin system had no major role in the establishment or maintenance of hypertension. 4. Mean arterial pressure was directly related to expansion of the extracellular fluid volume.

Pathophysiology of oedema in nephrotic syndrome

2015 ◽  
Author(s):  
Neil Turner ◽  
Premil Rajakrishna
Keyword(s):  
Nephrotic Syndrome ◽  
Osmotic Pressure ◽  
Serum Proteins ◽  
Collecting Duct ◽  
Extracellular Fluid ◽  
Colloid Osmotic Pressure ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Whole Body ◽  
Sodium Retention

The mechanism by which loss of serum proteins into the urine causes expansion of extracellular fluid volume and oedema has become clearer. A key initiating abnormality is avid sodium retention by the kidney, leading to increased whole-body sodium and increased extracellular fluid volume. This appears to be driven primarily by overactivation of the amiloride-sensitive epithelial sodium channel (ENaC) in the collecting duct, activated proteolytically through abnormal filtration of plasminogen, and its activation to plasmin in the nephron. Conventional explanations for nephrotic oedema focused on low colloid osmotic pressure as a consequence of loss of serum proteins, leading to egress of extracellular fluid from the intravascular compartment. It was hypothesized that this led to underfilling of the circulation and a drive to sodium retention. While low osmotic pressure may play a part in the clinical picture of nephrotic syndrome, a variety of observations suggest that underfilling is not a common feature except in the most severe nephrotic syndrome. Furthermore the gradient in colloid osmotic pressure between serum and interstitium tends to be preserved in nephrotic syndrome. The distribution of excess extracellular fluid is markedly different in patients with nephrotic syndrome from that seen in patients who have reduced glomerular filtration rate as the cause of sodium retention. This is not fully understood but hypotheses centre on capillary permeability and colloid osmotic pressure effects.

Effect of expansion of extracellular fluid volume on proximal sodium reabsorption in hyponatremic dogs

Metabolism ◽  
1970 ◽  
Vol 19 (4) ◽  
pp. 291-300 ◽  
Author(s):  
Bernard B. Davis ◽  
Franklyn G. Knox ◽  
Fred S. Wright ◽  
Stuart S. Howards
Keyword(s):  
Extracellular Fluid ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Sodium Reabsorption

The Value of Plasma Renin Concentration Per Se, and in Relation to Plasma and Extracellular Fluid Volume in Diagnosis and Prognosis of Human Renovascular Hypertension

1970 ◽  
Vol 39 (5) ◽  
pp. 559-576 ◽  
Author(s):  
G. Bianchi ◽  
L. Campolo ◽  
A. Vegeto ◽  
V. Pietra ◽  
U. Piazza
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Renal Disease ◽  
Renovascular Hypertension ◽  
Extracellular Fluid ◽  
Plasma Renin ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Plasma Renin Concentration ◽  
Diagnosis And Prognosis

1. Plasma renin concentration (PRC) has been measured in 212 hypertensive patients. In fourteen patients with essential hypertension and in seventeen patients with renovascular hypertension, plasma volume (PV) and extracellular fluid volume (ECFV) were measured. 2. The results obtained have been discussed in three ways: (a) PRC in relation to the aetiology of hypertension; (b) PRC in relation to the effect on blood pressure of surgery for unilateral renal diseases; (c) PRC, PV and ECFV in ‘essential’ and renovascular hypertension. 3. Excluding patients with ophthalmoscopic signs of malignant hypertension, PRC is significantly higher in renovascular hypertension than in normal subjects and patients suffering from ‘essential’ hypertension and hypertension associated with bilateral renal disease; but the overlapping of the single values of the patients with these diseases is marked. Thus a normal PRC has no diagnostic value, while a high PRC without sodium deficiency or retinopathy might favour a diagnosis of renovascular disease. 4. In twenty-seven out of thirty-three patients submitted to surgery for unilateral renal disease and followed up for 12 months or longer, blood pressure has been significantly reduced. This group includes twelve patients with a normal preoperative PRC and fifteen patients with a high PRC. These results clearly demonstrate that unilateral renal disease may maintain a high blood pressure without increasing PRC and that PRC has no prognostic value. 5. Concurrent estimations of PRC, PV and ECFV in patients with renovascular or essential hypertension revealed the following differences. In cases of renovascular hypertension with normal PRC, PV and ECFV were significantly increased while in those with raised PRC, PV did not differ and ECFV was barely raised with respect to values obtained in patients with essential hypertension. PV of renovascular patients with normal renin was significantly higher than that of renovascular patients with high renin. The analysis of these results with quadratic discriminant functions demonstrated that an integrated evaluation of blood pressure, PV, ECFV and PRC allows a separation between the two types of hypertension. In other words these factors, taken together, in some way seem to reflect a difference between the two diseases. These results may indicate a new type of approach to the diagnosis and prognosis of renovascular hypertension.

Suppression of the Renin—Aldosterone System in Mild Essential Hypertension

1976 ◽  
Vol 50 (4) ◽  
pp. 269-276
Author(s):  
A. M. Khokhar ◽  
J. D. H. Slater ◽  
T. P. Jowett ◽  
N. N. Payne
Keyword(s):  
Essential Hypertension ◽  
Plasma Renin Activity ◽  
Extracellular Fluid ◽  
Young Men ◽  
Plasma Renin ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Renin Activity ◽  
Low Renin Hypertension ◽  
Head Up Tilt

1. Suppression of the renin—aldosterone system by expansion of the extracellular fluid volume with extra sodium and mineralocorticoid for 6 days was studied in nine young men with very mild essential hypertension and in ten normotensive young men. 2. Plasma renin activity, measured both supine and after 45° head-up tilt, and the renal excretion of aldosterone 18-glucuronide were similar in both groups. However, after expansion of the extracellular fluid volume, hypertensive patients showed much less suppression of both variables. 3. This difference persisted despite matching for an equivalent degree of expansion of the extracellular fluid volume as indexed by the change in body weight. 4. Administration of extra sodium and mineralocorticoid produced a greater proportional fall of renal aldosterone excretion than of plasma renin activity in both groups and this dissociation was significantly more marked in the hypertensive group. 5. We suggest that (i) a relative autonomy of the renin—aldosterone system may be relevant to the pathogenesis and/or perpetuation of essential hypertension and (ii) that the syndrome of low-renin hypertension is unlikely to be associated with ‘mineralocorticoid’ excess.

scholarly journals Hemodynamic and hormonal changes during erythropoietin therapy in hemodialysis patients.

1998 ◽  
Vol 9 (1) ◽  
pp. 97-104
Author(s):  
M Lebel ◽  
I Kingma ◽  
J H Grose ◽  
S Langlois
Keyword(s):  
Cell Mass ◽  
Plasma Catecholamines ◽  
Extracellular Fluid ◽  
Plasma Renin ◽  
Hemodialysis Patients ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Hormonal Changes ◽  
Exchangeable Sodium ◽  
Total Blood

To better understand the mechanism of recombinant human erythropoietin (rhEPO)-induced increase in BP, hemodynamic parameters, body fluid volumes, and the hormones implicated in BP regulation were studied in 32 anemic hemodialysis patients before and after 3 to 4 mo of rhEPO therapy. Hemoglobin levels increased from 83 +/- 1.5 to 119 +/- 2.3 g/L (P < 0.01) after rhEPO therapy (25 to 43 U/kg) administered subcutaneously three times weekly. Mean 24-h systolic and diastolic ambulatory BP were significantly increased by 14 +/- 3 and 10 +/- 2 mmHg, respectively (P < 0.01 for both groups). Systemic vascular resistance consistently increased by 28 +/- 5% (P < 0.01), whereas cardiac output was decreased by 6 +/- 3% (P < 0.05). Red blood cell mass increased by 510 +/- 35 ml (P < 0.01), whereas plasma volume decreased by 420 +/- 66 ml (P < 0.01), which resulted in a nonsignificant increase in total blood volume. Extracellular fluid volume and exchangeable sodium were decreased by 873 +/- 255 ml (P < 0.01) and 125 mmol (P < 0.01), respectively. There was a positive correlation between the changes in exchangeable sodium and in systolic BP (r = 0.41, P < 0.05). Furthermore, a greater increase in 24-h systolic BP was observed in patients in whom exchangeable sodium increased or remained unchanged (n = 10) compared with patients (n = 22) with decreased exchangeable sodium (20 +/- 4 mmHg versus 8 +/- 2 mmHg, respectively, P < 0.01). Plasma catecholamines, plasma renin concentration, plasma atrial natriuretic peptide, and plasma endothelin-1 did not significantly change with rhEPO treatment, whereas plasma aldosterone increased significantly (P < 0.01). Although volume-independent mechanisms may contribute to rhEPO-induced BP increase, the results presented here suggest the importance of optimally reducing extracellular fluid volume to prevent, at least in part, the development of hypertension often observed with improved uremic anemia in these patients.

Separate roles of sodium ion concentration and fluid volumes in salt-loading hypertension in sheep

1975 ◽  
Vol 229 (4) ◽  
pp. 1068-1072 ◽  
Author(s):  
Norman RA ◽  
TG Coleman ◽  
Wiley TL ◽  
Manning RD ◽  
AC Guyton
Keyword(s):  
Extracellular Fluid ◽  
High Volume ◽  
Fluid Volume ◽  
Sodium Ion ◽  
Extracellular Fluid Volume ◽  
Ion Concentration ◽  
Sodium Retention ◽  
Salt Loading ◽  
High Sodium ◽  
Total Nephrectomy

The goal of these studies was to determine whether the hypertension caused by excessive salt loading results from sodium-induced expansion of the extracellular fluid volume or whether the salt increases the pressure in some other way, such as by causing vascular constriction. In one group of sheep, a combination of total nephrectomy and hemodialysis was used to produce and maintain step increases in extracellular fluid volume for 1 wk without a significant change in sodium ion concentration. In a 2nd group, unilateral nephrectomy, dialysis, and DOCA administration were used to cause step increases in sodium ion concentration while the extracellular fluid volume was held as close to normal as possible. The results showed a 41% increase in arterial pressure in the high-volume sheep and only a 4% increase in pressure in the high-sodium sheep. In both instances the total exchangeable sodium increased almost equally--a 21% increase in the high-sodium sheep. The data support the concept that sodium retention causes hypertension almost entirely because of sodium-induced expansion of the extracellular fluid volume.

Sign in / Sign up

Export Citation Format

Share Document