Relation between Plasma Aldosterone Concentration and Renal Handling of Sodium and Potassium, in Particular in Patients with Chronic Renal Failure

Nephron ◽  
1984 ◽  
Vol 37 (2) ◽  
pp. 94-99 ◽  
Author(s):  
Ronald J. Hené ◽  
Hendrik A. Koomans ◽  
Peter Boer ◽  
Jan C. Roos ◽  
Evert J. Dorhout Mees
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Plasma Aldosterone ◽  
Renal Handling ◽  
Plasma Aldosterone Concentration ◽  
Sodium And Potassium

Erythrocyte Sodium and Potassium during the Development of Chronic Renal Failure in Rats

1985 ◽  
Vol 69 (s12) ◽  
pp. 13P-13P
Author(s):  
T.H. Thomas ◽  
C. Mason ◽  
K.M. Illingworth
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Erythrocyte Sodium ◽  
Sodium And Potassium

Effects of routine heparin therapy on plasma aldosterone concentration

1991 ◽  
Vol 124 (3) ◽  
pp. 267-270 ◽  
Author(s):  
Yo Kageyama ◽  
Hiromichi Suzuki ◽  
Takao Saruta
Keyword(s):  
Plasma Cortisol ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Heparin Therapy ◽  
Plasma Aldosterone ◽  
The Other ◽  
Plasma Aldosterone Concentration ◽  
Low Sodium ◽  
Aldosterone Production ◽  
Sodium And Potassium

Abstract. Changes in plasma aldosterone, plasma renin activity, plasma cortisol, serum sodium and potassium concentrations were studied in 9 patients with thromboembolic diseases treated with heparin. Heparin was administered at doses of 700-1000 units/h for 7-10 days. Plasma aldosterone decreased from 239±33 to 114±25 pmol/l during heparin therapy and returned to basal levels after discontinuation of the therapy. In addition, responses to a low sodium intake (3 g/day) and ACTH were examined in 5 patients during and 2 weeks after heparin therapy. The increase in plasma aldosterone caused by low sodium intake was significantly attenuated during heparin therapy (124±5% increase from baseline) as compared with that 2 weeks after heparin therapy (148±7%, p<0.05). On the other hand, ACTH stimulated plasma aldosterone similarly during and at 2 weeks after heparin therapy (increase from baseline: 190±20% vs 193±9%). These results suggest that heparin decreased plasma aldosterone owing to attenuation of the angiotensin Il-induced aldosterone production.

Renal and adrenal responses to [des-Asp1]angiotensin I in the dog

1978 ◽  
Vol 234 (2) ◽  
pp. F130-F134 ◽  
Author(s):  
R. H. Freeman ◽  
J. O. Davis ◽  
M. C. Khosla
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Bolus Injection ◽  
Enzyme Inhibitor ◽  
Plasma Aldosterone ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Plasma Aldosterone Concentration ◽  
The Mean ◽  
Sodium And Potassium

There is evidence for the endogenous generation of [des-Asp1]angiotensin II (AIII) from a nonapeptide precursor, [des-Asp1]angiotensin I ([des-Asp1]AI). In the present study, the effects of equipressor doses of exogeneously administered [des-Asp1]AI and AIII on renal function and plasma aldosterone concentration were compared. Intravenous infusion of [des-Asp1]AI (75 ng/kg min-1 for 40 min) decreased renin secretion, renal blood flow, creatinine clearance, and sodium and potassium excretion in dogs. Infusion of AIII at one-third of the rate of [des-Asp1]AI (25 ng/kg min-1) produced comparable decreases in these same parameters. Filtration fraction was increased with both peptides. Both peptides also increased plasma aldosterone concentration to the same extent. A bolus injection (5 mg i.v.) of the converting enzyme inhibitor SQ 20,881 completely reversed the mean arterial pressure and renal blood flow responses to [des-Asp1]AI, but did not alter these responses to AIII. These data are consistent with the concept that endogenous generation of AIII from [des-Asp1]AI can occur via the action of converting enzyme on this substance.

URINARY EXCRETION OF SODIUM AND POTASSIUM IN RELATION TO PLASMA ALDOSTERONE CONCENTRATION

1972 ◽  
Vol 53 (3) ◽  
pp. 425-431 ◽  
Author(s):  
A. R. ADAMSON ◽  
S. W. JAMIESON
Keyword(s):  
Urinary Excretion ◽  
Low Dose ◽  
Urine Volume ◽  
Normal Subjects ◽  
Plasma Aldosterone ◽  
Urinary Sodium ◽  
Potassium Excretion ◽  
Plasma Aldosterone Concentration ◽  
Dose Infusion ◽  
Sodium And Potassium

SUMMARY The effect of a low dose infusion of aldosterone (7·0–8·4 ng/kg/min) on urinary sodium and potassium excretion was assessed in six normal subjects. Plasma aldosterone levels during these infusions (mean 38, range 23–62 ng/100 ml) compared favourably with levels obtained during Na+ deprivation (mean 38, range 30–46 ng/100 ml). In four paired experiments, aldosterone infused in this dose for 2 h produced a significant reduction in Na+ excretion (P < 0·01) and urine volume (P < 0·05) in the 4th hour after the start of the infusion compared with the control infusions. There was no significant change in K+ excretion. Prolonging the aldosterone infusion reduced Na+ excretion. A 10 h infusion of aldosterone (7·7 ng/kg/min) in one subject reduced Na+excretion to 6 μequiv./min. These results are compared to the levels of Na+ excretion obtained in dietary Na+ deprivation.

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