scholarly journals Relation between potassium balance and aldosterone secretion in normal subjects and in patients with hypertensive or renal tubular disease.

1966 ◽  
Vol 45 (6) ◽  
pp. 865-879 ◽  
Author(s):  
P J Cannon ◽  
R P Ames ◽  
J H Laragh
Keyword(s):  
Normal Subjects ◽  
Aldosterone Secretion ◽  
Potassium Balance ◽  
Renal Tubular ◽  
Renal Tubular Disease

A COMPARISON OF TWO METHODS FOR MEASUREMENT OF ALDOSTERONE SECRETION RATE IN MAN

1966 ◽  
Vol 53 (2) ◽  
pp. 177-188 ◽  
Author(s):  
P. Lund-Johansen ◽  
T. Thorsen ◽  
K. F. Støa
Keyword(s):  
Urinary Excretion ◽  
Normal Subjects ◽  
Secretion Rate ◽  
Aldosterone Secretion ◽  
Simple Method ◽  
Mean Values ◽  
Pathological Conditions ◽  
Significant Difference ◽  
Derivative Method ◽  
The Mean

ABSTRACT A comparison has been made between (A), a relatively simple method for the measurement of aldosterone secretion rate, based on paper chromatography and direct densitometry of the aldosterone spot and (B) a more elaborate isotope derivative method. The mean secretion rate in 9 normal subjects was 112 ± 26 μg per 24 hours (method A) and 135 ± 35 μg per 24 hours (method B). The »secretion rate« in one adrenalectomized subject after the intravenous injection of 250 μg of aldosterone was 230 μg per 24 hours (method A) and 294 μg per 24 hours (method B). There was no significant difference in the mean values, and correlation between the two methods was good (r = 0.80). It is concluded that the densitometric method is suitable for clinical purposes as well as research, being more rapid and less expensive than the isotope derivative method. Method A also measures the urinary excretion of the aldosterone 3-oxo-conjugate, which is of interest in many pathological conditions. The densitometric method is obviously the less sensitive and a prerequisite for its use is an aldosterone secretion of 20—30 μg per 24 hours. Lower values are, however, rare in adults.

Excretion of beta 2-glycoprotein I (apolipoprotein H) in renal tubular disease

1991 ◽  
Vol 37 (1) ◽  
pp. 74-77 ◽  
Author(s):  
A G W Norden ◽  
L M Fulcher ◽  
M Lapsley ◽  
F V Flynn
Keyword(s):  
Multiple Forms ◽  
Bence Jones Protein ◽  
Major Urinary Protein ◽  
Glycoprotein I ◽  
Apolipoprotein H ◽  
Beta 2 ◽  
Renal Tubular ◽  
Renal Tubular Disease ◽  
Urine Proteins ◽  
Tubular Proteins

Abstract beta 2-Glycoprotein I (beta 2GI) was identified as a major urinary protein excreted by patients with several renal tubular diseases, including adult Fanconi syndrome, nephrocalcinosis associated with autoimmune diseases, Lowe's syndrome, and Dent's disease (a familial renal tubular disease). Sixteen patients excreted between 2 and 40 mg of beta 2GI per millimole of creatinine. In contrast, 18 healthy controls had undetectable amounts of beta 2GI in urine. Isoelectric focusing followed by immunoblotting demonstrated multiple forms of beta 2GI with pls between 6.4 and 8.2. These pls are higher than for several other "tubular proteins"; beta 2GI may therefore be less retarded than more-anionic proteins by the glomerular charge-barrier. This could explain why large quantities of beta 2GI are excreted despite its relatively high molecular mass (50 kDa). Excretion of beta 2GI was easily demonstrated by routine electrophoresis of urine proteins. beta 2GI migrates in the beta-gamma region and may be confused with Bence Jones protein. beta 2GI is stable for at least two years in urine frozen at -25 degrees C.

scholarly journals Altered potassium balance and aldosterone secretion in a mouse model of human congenital long QT syndrome

2001 ◽  
Vol 98 (15) ◽  
pp. 8792-8797 ◽  
Author(s):  
I. Arrighi ◽  
M. Bloch-Faure ◽  
F. Grahammer ◽  
M. Bleich ◽  
R. Warth ◽  
...  
Keyword(s):  
Mouse Model ◽  
Long Qt Syndrome ◽  
Aldosterone Secretion ◽  
Long Qt ◽  
Potassium Balance ◽  
Qt Syndrome ◽  
Congenital Long Qt Syndrome

Potentiation of sulpiride-induced prolactin secretion by sodium deprivation in man

1980 ◽  
Vol 94 (1) ◽  
pp. 25-29 ◽  
Author(s):  
Masatomo Mori ◽  
Isao Kobayashi ◽  
Kihachi Ohshima ◽  
Sakae Maruta ◽  
Yohnosuke Shimomura ◽  
...  
Keyword(s):  
Control Diet ◽  
Normal Subjects ◽  
Sodium Content ◽  
Prolactin Secretion ◽  
Serum Prolactin ◽  
Aldosterone Secretion ◽  
Low Sodium Diet ◽  
Specific Radioimmunoassay ◽  
Prolactin Response ◽  
Pituitary Prolactin

Abstract. Previous studies suggest that prolactin is not an important osmoregulatory hormone in man, while aldosterone is well known to be important in osmoregulation. The present investigation was undertaken to ascertain whether serum osmotic changes affect pituitary prolactin secretion following sulpiride administration. Five normal subjects were placed on a constant isocaloric diet with different sodium content. Serum prolactin and aldosterone level were measured by specific radioimmunoassay. The basal serum level of prolactin was unaffected by changes in sodium content of the diet, in contrast to the basal level of aldosterone. On the other hand, the maximum levels of serum prolactin in response to sulpiride (50 mg, im) were significantly higher on a low sodium diet (3 g of salt/day) than on a control diet (12– 15 g of salt/day). When the content of diet changed from low salt to high salt (25 g of salt/day), sulpiride-induced prolactin response decreased, though it was not significantly lower than that on a control diet. However, sulpiride administration could not stimulate aldosterone secretion under any of the various sodium contents of the diet. The present study provides evidence that lowering of serum osmolarity stimulates serum prolactin response to sulpiride administration in man and this response is not modulated by aldosterone secretion.

ACTH Stimulation of Aldosterone Secretion in Normal Subjects and in Patients with Chronic Adrenocortical Insufficiency1

1967 ◽  
Vol 27 (4) ◽  
pp. 568-575 ◽  
Author(s):  
JOSEPH R. TUCCI ◽  
ERIC A. ESPINER ◽  
PAUL I. JAGGER ◽  
GEORGE L. PAUK ◽  
DAVID P. LAULER
Keyword(s):  
Normal Subjects ◽  
Aldosterone Secretion ◽  
Acth Stimulation ◽  
Stimulation Of

Control of aldosterone secretion by change of body potassium in normal man

1964 ◽  
Vol 207 (1) ◽  
pp. 104-108 ◽  
Author(s):  
Donald S. Gann ◽  
Catherine S. Delea ◽  
John R. Gill ◽  
J. Picton Thomas ◽  
Frederic C. Bartter
Keyword(s):  
Arterial Pressure ◽  
Plasma Volume ◽  
Normal Subjects ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Potassium Depletion ◽  
Intravascular Volume ◽  
Aldosterone Secretion ◽  
Body Sodium ◽  
Normal Man

Seven normal subjects were subjected to depletion and repletion of body potassium on balance regimen. Aldosterone excretion, plasma volume, and arterial pressure were measured. Potassium depletion decreased and potassium repletion consistently increased aldosterone excretion. Changes in sodium balance were prevented by restricting dietary sodium or replacing lost sodium. The effects on aldosterone excretion were thus shown to be independent of reciprocal changes in sodium balance of intravascular volume or of arterial pressure. The results suggest that changes in body potassium influence aldosterone secretion by mechanisms independent of those responsive to changes in body sodium or fluid volume.

Regulation of Angiotensin Receptors

Physiology ◽  
1986 ◽  
Vol 1 (2) ◽  
pp. 67-69 ◽  
Author(s):  
JG Douglas
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Cardiovascular Function ◽  
Angiotensin Receptors ◽  
Electrolyte Balance ◽  
Receptor Density ◽  
Angiotensin Receptor ◽  
Aldosterone Secretion ◽  
Potassium Balance ◽  
Stimulation Of

Angiotensin affects cardiovascular function through contraction of vascular smooth muscle and stimulation of aldosterone secretion, responses that are modulated by alterations in sodium or potassium balance. Changes in angiotensin receptor density of the target tissues are the major determinant of tissue responsiveness during alterations in electrolyte balance.

Renal Tubular Disease

2008 ◽  
pp. 193-211
Author(s):  
Russell W. Chesney
Keyword(s):  
Renal Tubular ◽  
Renal Tubular Disease
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