Determination of Plasma Renin Activity by Radioimmunoassay of Angiotensin I

1973 ◽  
Vol 44 (1) ◽  
pp. 43-54 ◽  
Author(s):  
S. Fukuchi ◽  
T. Takeuchi ◽  
T. Torikai
Keyword(s):  
Plasma Renin Activity ◽  
Simple Procedure ◽  
Plasma Renin ◽  
Inhibitory Effect ◽  
Renin Activity ◽  
Rabbit Serum ◽  
Chronic Glomerulonephritis ◽  
Angiotensin I ◽  
Standard Curve

1. A simple, rapid radioimmunoassay of angiotensin I has been applied to the measurement of plasma renin activity. 2. Antibody to angiotensin I was raised in rabbits by injecting angiotensin I conjugated with rabbit serum albumin. 3. Angiotensin I was generated in plasma by 3 h incubation at 37°C and pH 5.5 after adding EDTA and di-isopropylfluorophosphate (DFP). 4. The simple procedure of boiling for 10 min was performed to eliminate the inhibitory effect of plasma protein on immunoassay. After centrifugation, the supernatant was incubated for 18 h with 131I-labelled angiotensin I and antiserum. Free fractions of 131I-labelled angiotensin I were separated using dextran-coated charcoal, and compared with the standard curve. 5. Mean recovery of renin through the method was 91.8%; mean recovery of angiotensin I was 87.0%. 6. Normal values for plasma renin activity (estimated as the rate of generation of angiotensin I) was 1.17±0.90 ng ml−1 h−1; n = 21. Plasma renin activity was normal in essential hypertension; high in chronic glomerulonephritis with oedema; often high in renovascular hypertension; and low in primary aldosteronism.

Faster radioimmunoassay of angiotensin I at 37 degrees C.

1978 ◽  
Vol 24 (1) ◽  
pp. 115-118 ◽  
Author(s):  
F Fyhrquist ◽  
L Puutula
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Plasma Samples ◽  
Angiotensin I ◽  
Hypertensive Patients ◽  
Standard Curve ◽  
Analytical Recovery ◽  
Nonequilibrium Conditions ◽  
Working Day

Abstract We applied a 1-h radioimmunoassay incubation at 37 degrees C in determining generated angiotensin I in an assay for plasma renin activity. Under these nonequilibrium conditions, 26% of the 125I-labeled angiotensin I was bound at zero dose of unlabeled angiotensin, as compared to 57% at equilibrium after 18 h at 4 degrees C. Sensitivity and useful range for the standard curve remained unchanged. Blanks were not altered. There was a good (r = .971) correlation between renin values in 120 plasma samples from hypertensive patients as measured with both procedures. With isoelectric focusing, we detected no damage to the labeled angiotensin I during incubation for 1 h at 37 degrees C in the presence of diluted plasma, disodium ethylenediaminetetraacetate, hydroxyquinoline, and neomycin. Analytical recovery of unlabeled angiotensin I added to the assay mixture was 98 +/- 2.3% (mean +/- SD). We conclude that our incubation conditions allow rapid and accurate assay of plasma renin activity to be completed in one working day.

RADIOIMMUNOLOGICAL DETERMINATION OF PLASMA RENIN ACTIVITY DURING THE MENSTRUAL CYCLE AND DURING ACUTE PROGESTERONE ADMINISTRATION

1971 ◽  
Vol 67 (1) ◽  
pp. 174-186 ◽  
Author(s):  
Johan A. Sundsfjord
Keyword(s):  
Menstrual Cycle ◽  
Plasma Renin Activity ◽  
Limit Of Detection ◽  
Plasma Renin ◽  
Renin Activity ◽  
Angiotensin I ◽  
Sephadex Column ◽  
Radioimmunological Determination ◽  
Iodine 125

ABSTRACT Antibodies to ileu5angiotensin I were produced in rabbits with the poly-l-lysine succinyl complex of angiotensin I. Iodine-125 was used for the labelling of angiotensin I. The tracer was purified on a G-15 Sephadex column. For the determination of plasma renin activity plasma samples containing EDTA and BAL were incubated for two hours at 37°C. while a parallel sample was kept at 4°C to serve as a plasma blank. The angiotensin I content in 50 μl of plasma diluted 1:20 was quantitated directly, without prior extraction. For the immunoassay the samples and standards were incubated with 125I-angiotensin I (about 2500 cpm) and antiserum at a final dilution of 1:50 000–1:60 000 for 16–18 hours at 4°C. Dextran-coated charcoal was used for the separation of free and antibody-bound angiotensin I. The antiserum did not bind angiotensin II. The lower limit of detection was 20 pg. An average recovery of added angiotensin I of 100.5 % ± 11 (sd) was obtained. In duplicate determinations a coefficient of variation of 6.9 % was found. The method was used to measure renin activity during the menstrual cycle. In the follicular phase a range of 0.8–1.5, mean 1.14 ng ang.I/ml/h, was found, whereas the values in the luteal phase were 2.1–4.0, mean 3.06 ng ang.I/ml/h, respectively. When 500 mg progesterone, divided into 5 doses over a period of 24 hours was given to menopausal women, an increase in renin activity was found. No increase in aldosterone excretion or in the K/Na ratio in the urine was observed during this period.

VARIATIONS IN PLASMA RENIN ACTIVITY AND URINARY ALDOSTERONE EXCRETION IN NORMAL SUBJECTS AFTER SALT RESTRICTION AND ACUTE PITUITARY INHIBITION WITH 6-DEHYDRO-16-METHYLENE HYDROCORTISONE

1971 ◽  
Vol 67 (1) ◽  
pp. 159-173
Author(s):  
A. Peytremann ◽  
R. Veyrat ◽  
A. F. Muller
Keyword(s):  
Plasma Renin Activity ◽  
Salt Intake ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Inhibitory Effect ◽  
Renin Activity ◽  
Sodium Balance ◽  
Experimental Conditions ◽  
Salt Restriction ◽  
Aldosterone Production

ABSTRACT Variations in plasma renin activity and urinary aldosterone excretion were studied in normal subjects submitted to salt restriction and simultaneous inhibition of ACTH production with a new synthetic steroid, 6-dehydro-16-methylene hydrocortisone (STC 407). At a dose of 10 mg t. i. d. this preparation exerts an inhibitory effect on the pituitary comparable to that of 2 mg of dexamethasone. In subjects maintained on a restricted salt intake, STC 407 does not delay the establishment of an equilibrium in sodium balance. The increases in endogenous aldosterone production and in plasma renin activity are also similar to those seen in the control subjects. A possible mineralocorticoid effect of STC 407 can be excluded. Under identical experimental conditions, the administration of dexamethasone yielded results comparable to those obtained with STC 407.

Effect of enalapril (MK-421), an orally active angiotensin I converting enzyme inhibitor, on blood pressure, active and inactive plasma renin, urinary prostaglandin E2, and kallikrein excretion in conscious rats

1984 ◽  
Vol 62 (1) ◽  
pp. 116-123 ◽  
Author(s):  
Ernesto L. Schiffrin ◽  
Jolanta Gutkowska ◽  
Gaétan Thibault ◽  
Jacques Genest
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Ace Inhibition ◽  
Renin Activity ◽  
Prostaglandin E ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Angiotensin I Converting Enzyme

The angiotensin I converting enzyme (ACE) inhibitor enalapril (MK-421), at a dose of 1 mg/kg or more by gavage twice daily, effectively inhibited the pressor response to angiotensin I for more than 12 h and less than 24 h. Plasma renin activity (PRA) did not change after 2 or 4 days of treatment at 1 mg/kg twice daily despite effective ACE inhibition, whereas it rose significantly at 10 mg/kg twice daily. Blood pressure fell significantly and heart rate increased in rats treated with 10 mg/kg of enalapril twice daily, a response which was abolished by concomitant angiotensin II infusion. However, infusion of angiotensin II did not prevent the rise in plasma renin. Enalapril treatment did not change urinary immunorcactive prostaglandin E2 (PGE2) excretion and indomethacin did not modify plasma renin activity of enalapril-treated rats. Propranolol significantly reduced the rise in plasma renin in rats receiving enalapril. None of these findings could be explained by changes in the ratio of active and inactive renin. Water diuresis, without natriuresis and with a decrease in potassium urinary excretion, occurred with the higher dose of enalapril. Enalapril did not potentiate the elevation of PRA in two-kidney one-clip Goldblatt hypertensive rats. In conclusion, enalapril produced renin secretion, which was in part β-adrenergically mediated. The negative short feedback loop of angiotensin II and prostaglandins did not appear to be involved. A vasodilator effect, apparently independent of ACE inhibition, was found in intact conscious sodium-replete rats.

scholarly journals Estimation of the efficacy of the measurement of plasma renin activity and direct renin in diagnostics of primary aldosteronism

2012 ◽  
Vol 58 (5) ◽  
pp. 21-27
Author(s):  
N P Goncharov ◽  
G S Kolesnikova ◽  
G V Katsiia ◽  
E Iu Rogal'
Keyword(s):  
Plasma Renin Activity ◽  
Primary Aldosteronism ◽  
Plasma Renin ◽  
Pressure Control ◽  
Renin Activity ◽  
Differential Diagnostics ◽  
Control Groups ◽  
Aldosterone Level ◽  
Renin Level

The objective of the present study was to estimate the informative value of the measurements of aldosterone level, direct renin, and plasma renin activity as well as the relationships between these characteristics for differential diagnostics of various forms of hypertension and, first and foremost, of primary aldosteronism. We have examined a total of 162 patients. The results of differential tests were used to allocate them to a few groups including 41 patients presenting with primary aldosteronism, 52 ones with incidentalomas, 26 with essential hypertension, and 43 with various endocrine diseases and normal arterial pressure (control groups). The aldosterone levels, direct renin, and plasma renin activity were measured in blood samples taken in morning hours from the patients in the supine position. The aldosterone to plasma renin activity (A/PRA) and aldosterone to direct renin (A/DR) ratios were calculated. The elevated blood aldosterone level is currently believed to be the principal criterion for primary aldosteronism in the patients suffering arterial hypertension. The RIA technology is the method of choice for the measurement of aldosterone levels. The determination of the A/PR ratio significantly improves the detectability of the disease. The use of direct renin level instead of kinetic renin ensures the high efficacy of screening for primary aldosteronism and its early diagnostics. The cut-off point for the calculation of the A/PRA ratio to differentiate between primary aldosteronism and incidentalomas is 2160 pmol/mcg/hr (sensitivity 100%, specificity 97.8%) in comparison with the analogous cut-off point for the discrimination between primary aldosteronism and endocrine pathology without hypertension is 49 pmol/mU (sensitivity 100%, specificity 95%). The cut-off point for the calculation of the A/PR ratio to differentiate between primary aldosteronism and incidentalomas is 2160 pmol/mcg/hr (sensitivity 89.5%, specificity 99%) in comparison with the analogous cut-off point for the discrimination between primary aldosteronism and endocrine pathology without hypertension is 1432 pmol/mcg/hr (sensitivity 89.5%, specificity 100%). It is concluded that the results of determination of direct renin level in the blood plasma are independent of the endogenous angiotensinogen level, less variable and more reproducible than than the results of the measurement of plasma renin activity. The aldosterone to direct renin ratio may be used for the screening of primary aldosteronism.

Micro-determination of human plasma renin activity with the addition of homologous substrate

1968 ◽  
Vol 22 (3) ◽  
pp. 309-315 ◽  
Author(s):  
Kikuo Arawaka ◽  
Atsushi Minohara ◽  
Junko Yamada ◽  
Nobuhiro Uemura ◽  
Motoomi Nakamura
Keyword(s):  
Plasma Renin Activity ◽  
Human Plasma ◽  
Plasma Renin ◽  
Renin Activity ◽  
Homologous Substrate

Plasma Renin Activity and Plasma Renin Substrate in Hypertension Associated with Steroid Excess

1973 ◽  
Vol 45 (s1) ◽  
pp. 295s-299s ◽  
Author(s):  
L. R. Krakoff ◽  
M. Mendlowitz
Keyword(s):  
Oral Contraceptive ◽  
Plasma Renin Activity ◽  
Cushing’S Syndrome ◽  
Plasma Renin ◽  
Cushing's Syndrome ◽  
Glucocorticoid Therapy ◽  
Renin Activity ◽  
Angiotensin I ◽  
Renin Substrate ◽  
Contraceptive Agents

1. Plasma renin activity and plasma renin substrate were measured by radioimmunoassay of generated angiotensin I in patients with steroid excess syndromes. Significant increases in substrate were observed in patients with Cushing's syndrome, during glucocorticoid therapy and on oral contraceptive agents. Suppression of plasma renin activity occurred only in primary aldosteronism. 2. The Michaelis constant (Km) for the reaction between renin and substrate in plasma at physiological pH (7.4) was also determined. The extent to which elevated plasma renin substrate increases the velocity of angiotensin I formation was then calculated. 3. In patients with Cushing's syndrome, glucocorticoid therapy or oral contraceptive use, elevated renin substrate coupled with failure of suppression of circulating renin results in increased angiotensin I formation.

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