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.

Basal and saline-stimulated plasma atrial natriuretic hormone in Cushing's syndrome

1991 ◽  
Vol 124 (1) ◽  
pp. 7-11 ◽  
Author(s):  
J. A. McKnight ◽  
D. R. McCance ◽  
G. Roberts ◽  
B. Sheridan ◽  
A. B. Atkinson
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Cushing’S Syndrome ◽  
Plasma Renin ◽  
Cushing's Syndrome ◽  
Renin Activity ◽  
Natriuretic Hormone ◽  
Serum Aldosterone ◽  
Atrial Natriuretic Hormone ◽  
Atrial Natriuretic

Abstract. The pathogenesis of hypertension associated with Cushing's syndrome is incompletely understood. We have studied basal and saline-stimulated levels of plasma atrial natriuretic hormone in 10 subjects with active Cushing's syndrome (8 F: 2 M), aged 43±4 years (mean±sem). Ten age- and sex-matched normal control subjects were also studied. Subjects fasted from 22.00 h, rose at 07.45 h, and remained ambulant until 09.45 h when blood was taken for plasma ANH, plasma renin activity and serum aldosterone. Subjects then rested supine until 10.00 h when blood was again taken, and blood pressure recorded. Then, while subjects remained supine, 2 1 of 0.9% NaCl were infused between 10.00 and 14.00 h. Blood was taken hourly. Basal plasma ANH was 8.0±0.9 pmol/l in Cushing's subjects and 6.9±2.5 pmol/l in controls. Levels increased in response to saline in both groups, and became significantly higher in the group of patients with Cushing's syndrome (14.00 h level 21.3±3.9 vs 10.4± 1.9 pmol/l; p<0.05). Serum aldosterone and plasma renin activity were not different between groups. Mean blood pressure was higher in patients (114±4 vs 91±7 mmHg; p<0.05). Urinary sodium excretion was not different between groups before saline, but during the four hours of saline was higher in Cushing's subjects (133±12 vs 67±11 mmols; N=6; p<0.05). Our results suggest that during salt loading the exaggerated natriuresis seen in the Cushing's group may have been caused by ANH.

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.

Plasma renin activity and plasma prorenin assays

1991 ◽  
Vol 37 (10) ◽  
pp. 1811-1819 ◽  
Author(s):  
J E Sealey
Keyword(s):  
Plasma Renin Activity ◽  
Sodium Intake ◽  
Vascular Complications ◽  
Plasma Renin ◽  
Renin Activity ◽  
Blood Collection ◽  
Kinetic Assay ◽  
Renin Substrate ◽  
Patients With Diabetes ◽  
Commercial Kits

Abstract Sensitivity and accuracy are essential features of an assay of plasma renin activity (PRA) because the normal concentration of PRA is only 1 pmol/L, and subnormal concentrations have diagnostic relevance. Conditions for blood collection need to be standardized but the conditions are not difficult for outpatients. For routine diagnostic purposes blood should be collected from ambulatory (ideally, untreated) patients on moderate sodium intake. To avoid irreversible cryoactivation of plasma prorenin (which is present in 10-fold greater concentrations than renin), samples should be processed at room temperature and stored completely frozen. Cryoactivation occurs when plasma is liquid at temperatures less than 6 degrees C. PRA is commonly measured with an enzyme kinetic assay in which angiotensin I (Ang I) is formed by the reaction of plasma renin with endogenous renin substrate (angiotensinogen). The Ang I so formed is measured by RIA; results are expressed as an hourly rate (micrograms/L formed per hour). This method, which is provided by most commercial kits, has the potential for unlimited sensitivity because the step for Ang I generation can be prolonged as long as necessary, so that enough Ang I forms to be measured accurately. Unfortunately, that sensitivity is not always exploited. Dilution of plasma during pH adjustment should be kept to a minimum. The Ang I generation step should last at least 3 h. The step should last 18 h for samples with PRA less than 1.0 micrograms/L per hour, to eliminate the errors inherent in the measurement and subtraction of immunoreactive Ang I in the untreated plasma (blank subtraction). These changes actually simplify PRA measurements because they eliminate the need for ice in the clinic and reduce by almost half the number of samples to be assayed by RIA. I also describe the method for measurement of plasma prorenin, which may be an important marker for patients with diabetes mellitus who subsequently develop vascular complications.

Measurement of Plasma Renin Activity as a Valid Estimation of Plasma Angiotensin Status

1978 ◽  
Vol 15 (1-6) ◽  
pp. 250-252 ◽  
Author(s):  
J. E. Roulston ◽  
G. A. Macgregor ◽  
Theresa Adam ◽  
Nirmala D. Markandu
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Activity Measurement ◽  
Plasma Samples ◽  
Angiotensin I ◽  
Plasma Angiotensin ◽  
Rate Limiting

Measurement of plasma renin activity is widely used as an indirect assessment of plasma angiotensin II concentration. There has been some controversy over the validity of this assay as an estimate of circulating angiotensin II levels because, during the in vitro generation of angiotensin I by renin, over a period of time, substrate concentration may diminish to such an extent that it becomes rate-limiting, giving an artificially low reflection of angiotensin II levels. In this paper the initial angiotensin I concentration, that is the concentration before in vitro angiotensin I generation, has been compared with the corresponding plasma renin activity for 2752 individual plasma samples. A linear relationship was found between the initial angiotensin I concentration and the plasma renin activity below 60 ng ml−1 h−1. This indicates that, under the conditions of this assay, substrate does not appear to become rate-limiting except at exceedingly high levels of plasma renin activity. These results appear to provide further validation for the use of plasma renin activity measurement as a reflection of the concentration of circulating angiotensin II levels.

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.

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