Effects of ACEI and low sodium intake on the renin–angiotensin system in mice with unilateral hydronephrosis

2009 ◽  
Vol 137 ◽  
pp. S93
Author(s):  
Y.L. ZHANG ◽  
J.Y. WU ◽  
X.C. WANG ◽  
X.A. JING
Keyword(s):  
Sodium Intake ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Low Sodium ◽  
Unilateral Hydronephrosis

Aldosterone escape to chronic ACTH administration in man

1983 ◽  
Vol 103 (1) ◽  
pp. 116-124 ◽  
Author(s):  
Rolf C. Gaillard ◽  
Anne M. Riondel ◽  
Charles A. Favrod-Coune ◽  
Michel B. Vallotton ◽  
Alex F. Muller
Keyword(s):  
Sodium Intake ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Aldosterone Secretion ◽  
Acth Stimulation ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Refractory State

Abstract. Prolonged ACTH administration produces a transient and self-limiting stimulation of aldosterone secretion which has been attributed to sodium retention, to inhibition of final enzymatic steps of aldosterone biosynthesis and/or to a morphological change of the glomerulosa cells. This study was undertaken to determine the possible role of the renin-angiotensin system in mediating the aldosterone escape to repeated ACTH stimulation. We studied in normal male volunteers the effect of a 4 day ACTH administration on urinary aldosterone metabolite excretion (3 oxo-conjugate and tetrahydroaldosterone) during concomitant diuretic administration (spironolactone or triamterene). In addition the plasma aldosterone response to acute iv stimulation with ACTH before and during the corticotrophin-induced 'refractory state' was examined both on normal and on low sodium diet. Spironolactone was unable to counteract the sodium retention induced by ACTH stimulation; aldosterone excretion showed the same transient increase as with ACTH alone while plasma renin activity remained low. Triamterene produced a negative sodium balance, a significantly more sustained increase in aldosterone excretion and an increase in plasma renin activity. In either situation the two metabolites of aldosterone showed the same pattern of excretion. The plasma aldosterone response to acute iv ACTH stimulation was completely blocked during the corticotrophin-induced 'refractory state' on normal sodium intake, whereas on low sodium diet a clear-cut response was still obtained. These data suggest that the transient effect of ACTH on aldosterone secretion is dependent on the state of activity of the renin-angiotensin system. When renin was stimulated by low sodium intake or sodium depletion, the aldosterone response to repeated ACTH administration was more sustained, and when renin was stimulated by low sodium intake, the aldosterone response to acute ACTH was maintained. In conclusion we suggest that the renin-angiotensin system is able to delay but not to suppress the changes induced in the zona glomerulosa by prolonged ACTH stimulation.

Angiotensin augments epinephrine release in pithed rats fed a low-sodium diet

1990 ◽  
Vol 258 (1) ◽  
pp. R187-R192 ◽  
Author(s):  
R. R. Vollmer ◽  
S. P. Corey ◽  
S. A. Meyers ◽  
E. M. Stricker ◽  
S. J. Fluharty
Keyword(s):  
Angiotensin Ii ◽  
Sodium Intake ◽  
Renin Angiotensin System ◽  
Dietary Sodium ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Pithed Rats

In confirmation of previous studies, the amount of epinephrine released into blood during electrical stimulation of the thoracolumbar region of the spinal cord in pithed rats on a low-sodium diet (0.01% sodium by weight of diet for 1 mo) was significantly greater than that observed in rats on a normal sodium diet (0.3% sodium by weight of diet). The present work assessed the extent to which endogenously formed angiotensin II influences this neurally mediated adrenal epinephrine release. The augmented release of epinephrine in rats maintained on the low-sodium diet appeared to depend on circulating angiotensin II because blockade of angiotensin II receptors with saralasin decreased the epinephrine release in these animals but not in rats maintained on the normal diet. Similar results were obtained when the renin-angiotensin system was blocked with the converting-enzyme inhibitor captopril. Adrenal epinephrine content was not affected by the dietary sodium intake; however, the catecholamine synthetic capacity was augmented as indicated by a significant induction of tyrosine hydroxylase. In addition, the adrenal medullary angiotensin II receptor density was significantly elevated in animals on the low-sodium diet. These results demonstrate that endogenous angiotensin II is capable of providing a positive modulatory influence on neurally mediated release of adrenal epinephrine, an effect that may require a chronic activation of the renin-angiotensin system as occurs naturally with restricted dietary sodium intake.

Neurohumoral Response to Hospitalization in Hypertensive Patients

1981 ◽  
Vol 61 (s7) ◽  
pp. 385s-387s ◽  
Author(s):  
P. W. De Leeuw ◽  
G. A. W. Van Soest ◽  
R. Punt ◽  
R. P. L. M. Hoogma ◽  
A. J. P. M. Smout ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sodium Intake ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Group 2 ◽  
Reduced Activity ◽  
Hypotensive Response ◽  
Group 1 ◽  
Noradrenaline Levels

1. To investigate whether reduced activity of pressor systems could explain the spontaneous drop in pressure upon hospitalization, 51 subjects with uncomplicated essential hypertension were admitted to hospital. Sodium intake was fixed at 55 mmol/day. 2. Blood samples for noradrenaline, adrenaline, active renin, angiotensin II and aldosterone were drawn on each morning of the first 3 days of hospitalization; blood pressure was measured at 2 h intervals and values were averaged for each day. 3. Subjects were divided in two groups depending on whether they became normotensive (group 1; n = 12) or remained hypertensive (group 2; n = 39). This distinction was thought to reflect mild and more severe hypertensive groups respectively. 4. Although both groups showed a comparable fall in blood pressure during hospitalization, noradrenaline levels fell more consistently in group 1, whereas adrenaline levels fell only in group 2. The components of the renin—angiotensin—aldosterone system rose, but more conspicuously in group 1. 5. It is concluded that withdrawal of sympathetic activity can only partly explain the hypotensive response to hospitalization. The renin—angiotensin system behaves only passively and appears to be counterproductive to alterations in blood pressure.

Role of the renin-angiotensin system in potassium control

1980 ◽  
Vol 238 (5) ◽  
pp. R359-R363
Author(s):  
D. B. Young ◽  
R. E. McCaa
Keyword(s):  
Potassium Concentration ◽  
Renin Angiotensin System ◽  
Plasma Potassium ◽  
Sodium Balance ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Low Sodium ◽  
Group I ◽  
Urinary Potassium ◽  
Group Ii

To determine the importance of the renin-angiotensin system in control of plasma potassium concentration and excretion, potassium control was studied in two groups of dogs in response to a 20-fold increase in sodium intake (from 10 to 200 meq/day). Group I was intact whereas group II lacked feedback control of the renin-angiotensin system, which was eliminated by continuous infusion of 10 ng . kg-1 . min-1 angiotensin II. This rate of infusion reduced endogenous plasma renin activity (PRA) to undetectable levels throughout the study. The sodium forcing did not result in measurable changes in plasma potassium concentration or excretion in group I, in which PRA fell to 40% and plasma aldosterone concentration (PAC) to 60% of the low sodium levels. In group II the same sodium forcing produced a 12% decrease in plasma potassium concentration and a 79% increase in urinary potassium excretion. PAC also fell to 60% of the low sodium level in group II. The results demonstrate the importance of the renin-angiotensin system as a link between the nephron and the zona glomerulosa that is essential in controlling plasma potassium concentration and excretion during changes in sodium balance.

Role of the Renin-Angiotensin System in the Regulation of Late Steps in Aldosterone Biosynthesis by Sodium Intake of Potassium-Deficient Rats*

Endocrinology ◽  
1984 ◽  
Vol 115 (1) ◽  
pp. 350-356 ◽  
Author(s):  
JÜRG MÜLLER, ◽  
LILIAN HOFSTETTER ◽  
PATRICIA SCHWENDENER-CANLAS ◽  
DORETTE B. BRUNNER ◽  
EVA-GRETHE LUND
Keyword(s):  
Sodium Intake ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin

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.

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