Plasma renin activity and plasma aldosterone in acute renal failure

1980 ◽  
Vol 12 (1) ◽  
pp. 83-90
Author(s):  
M. Mydlík ◽  
K. Horký ◽  
P. Jonáš ◽  
I. Gregorová ◽  
I. Macháňová ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity

Failure of Loading with Sodium Bicarbonate to Protect against Acute Renal Failure Induced by Mercuric Chloride in the Rat

1977 ◽  
Vol 53 (2) ◽  
pp. 149-154 ◽  
Author(s):  
J. E. Beaumont ◽  
T. A. Kotchen ◽  
J. H. Galla ◽  
R. G. Luke
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Sodium Balance ◽  
Control Group ◽  
Sprague Dawley ◽  
Urinary Volume ◽  
Sprague Dawley Rats

1. To investigate the mechanism by which sodium loading protects against acute renal failure we compared the effects of prior chronic loading with NaCl, or with NaHCO3, on renal function after injection of HgCl2. 2. Twenty-four male Sprague-Dawley rats were divided into three groups of eight rats. One group drank isotonic NaCl solution, a second drank isotonic NaHCO3 solution and the third control group drank deionized water. Acute renal failure was induced by HgCl2 on day 9, and the rats were killed 48 h after injection. 3. Net sodium balances and plasma volumes were similar in both groups of sodium-loaded rats. After HgCl2 serum creatinine was significantly less and urinary volume was greater in NaCl-loaded than in both NaHCO3-loaded and water-drinking animals. 4. Plasma renin activity of both NaCl- and NaHCO3-loaded animals was less than that of control rats. However, renal renin content was suppressed by NaCl but not by NaHCO3 loading. 5. Loading with NaCl afforded greater protection against HgCl2-induced acute renal failure than NaHCO3. Since this difference was not related to changes in sodium balance or plasma volume before HgCl2, or plasma renin activity after HgCl2, the results support the hypothesis that intrarenal renin plays a role in the pathogenesis of HgCl2-induced acute renal failure in the rat.

Plasma renin activity in folic acid induced acute renal failure

1972 ◽  
Vol 50 (16) ◽  
pp. 797-798 ◽  
Author(s):  
U. Helmchen ◽  
Ursula Kneissler ◽  
Heide Fischbach ◽  
P. Reifferscheid ◽  
U. Schmidt
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Folic Acid ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity

scholarly journals Effects of prolonged infusion of basic fibroblast growth factor and IGF-I on adrenocortical differentiation in the autotransplanted adrenal: an immunohistochemical study

1999 ◽  
Vol 162 (1) ◽  
pp. 21-29 ◽  
Author(s):  
P Vendeira ◽  
D Pignatelli ◽  
D Neves ◽  
MM Magalhaes ◽  
MC Magalhaes ◽  
...  
Keyword(s):  
Growth Factors ◽  
Growth Factor ◽  
Plasma Renin Activity ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Fibroblast Growth ◽  
Igf I

Adrenocortical regeneration after adrenal autotransplantation provides a model for the study of local autocrine/paracrine mechanisms involved in the growth and differentiation of the adrenal cortex. To study the possible involvement of some growth factors, namely basic fibroblast growth factor (bFGF, FGF-2) and insulin-like growth factor I (IGF-I), in cell differentiation, immunohistochemical and ultrastructural studies were carried out on adrenal autotransplants in adult male rats. To distinguish between fasciculata and glomerulosa-like cells with accuracy, tissue sections were immunostained with IZAb, which recognizes the inner zone antigen (IZAg) present in fasciculata and reticularis cells but absent from the glomerulosa, and by electron microscopy. IGF-I-treated animals exhibited a clear glomerulosa-like zone that was devoid of IZAb immunostaining. In this outer subcapsular area, ultrastructural examination showed cells containing mitochondria with irregular cristae resembling those of the fetal or immature glomerulosa cells. In contrast, no significant morphological differences were observed in bFGF-treated animals when compared with those from saline-treated controls, in both of which, IZAb immunostaining occurred in almost all adrenocortical cells, with no clear zonation or glomerulosa, as seen in the intact animal. Plasma aldosterone and corticosterone concentrations were lower in autotransplanted control animals than in intact controls, although plasma renin activities were similar. IGF-I treatment significantly increased aldosterone concentrations, whereas corticosterone and plasma renin activity were reduced. bFGF infusion further reduced plasma aldosterone, although plasma renin activity and corticosterone were unaffected. These results suggest that the two growth factors have different effects on zonal differentiation and function in the autotransplanted gland. In particular, bFGF, by reducing glomerulosa function, appears partly to replicate the actions of ACTH in normal animals. In contrast, IGF-I enhances the glomerulosa secreting phenotype and diminishes that of the fasciculata/reticularis, possibly replicating the actions of angiotensin II or a low sodium diet.

Renin, aldosterone, electrolyte, and cortisol responses to hypoxic decompression

1977 ◽  
Vol 43 (3) ◽  
pp. 421-424 ◽  
Author(s):  
J. R. Sutton ◽  
G. W. Viol ◽  
G. W. Gray ◽  
M. McFadden ◽  
P. M. Keane
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Cortisol ◽  
Acute Mountain Sickness ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Plasma Sodium ◽  
Plasma Aldosterone Concentration ◽  
Urinary Potassium ◽  
Mountain Sickness

Responses of plasma renin activity, plasma aldosterone, plasma cortisol, and plasma electrolyte concentration and urinary electrolyte and aldosterone excretion were studied in four men during hypoxic decompression to a stimulated altitude of 4,760 m in a pressure chamber. Three of the four subjects developed significant acute mountain sickness. Plasma sodium and potassium concentrations were unchanged. No significant change in plasma renin activity was observed, but values tended to fall. Plasma aldosterone concentration was depressed while plasma cortisol was elevated and diurnal variation lost. Urinary sodium excretion was unchanged, but urinary potassium and aldosterone excretion were decreased. The decrease in plasma and urinary aldosterone and urinary potassium in the absence of change in plasma renin activity or plasma potassium is of uncertain origin. It is unlikely to be due to a decrease in adrenocorticotropin secretion since plasma cortisol rose during the same time. None of the changes could be causally implicated in the development of acute mountain sickness although the increase in plasma cortisol was greatest in the most ill.

The Effect of Weight Reduction on Blood Pressure, Plasma Renin Activity, and Plasma Aldosterone Levels in Obese Patients

1981 ◽  
Vol 304 (16) ◽  
pp. 930-933 ◽  
Author(s):  
Michael L. Tuck ◽  
James Sowers ◽  
Leslie Dornfeld ◽  
Gary Kledzik ◽  
Morton Maxwell
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Weight Reduction ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Obese Patients ◽  
Pressure Plasma

scholarly journals Effects of Ramipril on the Aldosterone/Renin Ratio and the Aldosterone/Angiotensin II Ratio in Patients With Primary Aldosteronism

Hypertension ◽  
2020 ◽  
Vol 76 (2) ◽  
pp. 488-496 ◽  
Author(s):  
Zeng Guo ◽  
Marko Poglitsch ◽  
Diane Cowley ◽  
Oliver Domenig ◽  
Brett C. McWhinney ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Ace Inhibitors ◽  
Primary Aldosteronism ◽  
Characteristic Curve ◽  
False Negative ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Plasma Aldosterone Concentration

The aldosterone/renin ratio (ARR) is currently considered the most reliable approach for case detection of primary aldosteronism (PA). ACE (Angiotensin-converting enzyme) inhibitors are known to raise renin and lower aldosterone levels, thereby causing false-negative ARR results. Because ACE inhibitors lower angiotensin II levels, we hypothesized that the aldosterone/equilibrium angiotensin II (eqAngII) ratio (AA2R) would remain elevated in PA. Receiver operating characteristic curve analysis involving 60 patients with PA and 40 patients without PA revealed that the AA2R was not inferior to the ARR in screening for PA. When using liquid chromatography-tandem mass spectrometry to measure plasma aldosterone concentration, the predicted optimal AA2R cutoff for PA screening was 8.3 (pmol/L)/(pmol/L). We then compared the diagnostic performance of the AA2R with the ARR among 25 patients with PA administered ramipril (5 mg/day) for 2 weeks. Compared with basally, plasma levels of equilibrium angiotensin I (eqAngI) and direct renin concentration increased significantly ( P <0.01 or P <0.05) after ramipril treatment, whereas eqAngII and ACE activity (eqAngII/eqAngI) decreased significantly ( P <0.01). The changes of plasma renin activity and plasma aldosterone concentration in the current study were not significant. On day 14, 4 patients displayed false-negative results using ARR_direct renin concentration (plasma aldosterone concentration/direct renin concentration), 3 of whom also showed false-negative ARR_plasma renin activity (plasma aldosterone concentration/plasma renin activity). On day 15, 2 patients still demonstrated false-negative ARR_plasma renin activity, one of whom also showed a false-negative ARR_direct renin concentration. No false-negative AA2R results were observed on either day 14 or 15. In conclusion, compared with ARR which can be affected by ACE inhibitors causing false-negative screening results, the AA2R seems to be superior in detecting PA among subjects receiving ACE inhibitors.

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