Letters to the Editor

PEDIATRICS ◽  
1981 ◽  
Vol 67 (2) ◽  
pp. 310-310
Author(s):  
Clarence E. Grim
Keyword(s):  
Plasma Renin Activity ◽  
Serum Potassium ◽  
Potassium Level ◽  
Plasma Renin ◽  
Renin Activity ◽  
Angiotensin I ◽  
Letters To The Editor

The comments by Dr Walson raise some worthwhile points. The level of serum potassium in each patient was measured on nine separate days. In only one patient (the youngest) was a single potassium level of less than 3.6 mEq/liter obtained. Thus, in 26 of 27 measurements, potassium was normal (96% of the time). In contrast, plasma renin activity (PRA) was always less than 0.5 ng of angiotensin I (AI) per ml per 3 hr in 17 of 17 samples collected (100%) on each patient.

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 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.

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.

Effect of Chronic Low-Dose Arginine Vasopressin Infusion on Body Fluid Homoeostasis during Adaptation from a High-to a Low-Sodium Diet in Normal Man

1993 ◽  
Vol 85 (4) ◽  
pp. 465-470 ◽  
Author(s):  
M. Sutters ◽  
D. J. S. Carmichael ◽  
S. L. Lightman ◽  
W. S. Peart
Keyword(s):  
Plasma Renin Activity ◽  
Arginine Vasopressin ◽  
Plasma Renin ◽  
Sodium Concentration ◽  
Renin Activity ◽  
Plasma Sodium ◽  
Angiotensin I ◽  
Salt Restriction ◽  
Plasma Sodium Concentration ◽  
Plasma Arginine

1. A diuresis occurs within the first 36 h of salt restriction. A decline in plasma arginine vasopressin concentration may contribute to both the diuresis and antinatriuresis. 2. We have studied six normal human subjects during 36 h of dietary sodium restriction. In one study subjects received an intravenous infusion of D-glucose, and in the other an infusion of arginine vasopressin (6 fmol min−1 kg−1). 3. In the D-glucose phase plasma arginine vasopressin concentration fell (1.77 +034 to 1.02 +0.13 pg/ml), urine flow increased (67.9 +113 to 89.8 + 17.1 ml/h), haemoconcentration occurred (packed cell volume 40.8 +0.3 to 42.8 +03%, protein concentration 71.6 +03 to 74.5 + 0.6 g/l), plasma sodium concentration fell (140 +0.2 to 138 +0.2 mmol/l) and plasma renin activity increased (1600+153 to 3700 + 356 pg of angiotensin I h−1 ml−1). 4. In the arginine vasopressin phase plasma arginine vasopressin concentration remained constant (13 + 0.13 to 134 +0.11 pg/ml), the diuresis was reversed (65.7 +9.9 to 52.1 +8.9 ml/h), plasma sodium concentration fell further (139.8 +0.4 to 136.1 +0.4 mmol/l), the rise in plasma renin activity was reduced (arginine vasopressin 2552 + 292; D-glucose, 3700 + 356 pg of angiotensin I h−1 ml−1) and creatinine clearance was lower in the last 12 h of salt restriction (arginine vasopressin, 96.1 +6.9; D-glucose 116.5 + 6.8 ml/min). Renal sodium excretion was unaffected by arginine vasopressin infusion. 5. We conclude that the fall in plasma arginine vasopressin concentration during dietary salt restriction, whilst not affecting renal sodium excretion, may be important in the regulation of plasma sodium concentration, plasma renin activity and glomerular filtration.

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.

Oestradiol-induced hypotension in spontaneously hypertensive rats: putative role for intracellular cations, sodium-potassium flux and prostanoids

1992 ◽  
Vol 82 (4) ◽  
pp. 389-395 ◽  
Author(s):  
C. Stonier ◽  
J. Bennett ◽  
E. A. Messenger ◽  
G. M. Aber
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Cell Volume ◽  
Packed Cell Volume ◽  
Spontaneously Hypertensive Rats ◽  
Plasma Renin ◽  
Renin Activity ◽  
Hypertensive Rats ◽  
Angiotensin I ◽  
Spontaneously Hypertensive

1. The effect of oestradiol alone and in combination with indomethacin on blood pressure, erythrocyte cation concentration and Na+−K+ flux has been studied in adult female normotensive and spontaneously hypertensive rats. 2. Oestradiol alone resulted in a significant decrease in blood pressure in spontaneously hypertensive rats (from 165.3 ± 3.9 to 146.4 ± 2.7 mmHg, P < 0.001), whereas it induced a significant increase in normotensive rats (from 111.8 ± 1.8 to 124.1 ± 3.6 mmHg, P < 0.001). When indomethacin and oestradiol were administered simultaneously or when indomethacin was given alone, no change in blood pressure occurred in spontaneously hypertensive rats (158.6 ± 6.9 and 159.8 ± 6.2 mmHg, respectively). 3. The fall in blood pressure induced by oestradiol in spontaneously hypertensive rats was associated with significant reductions in erythrocyte K+ concentration (from 127.4 ± 1.2 to 116.9 ± 1.7 mmol/l of cells, P < 0.001), in erythrocyte Na+ concentration (from 14.3 ± 0.8 to 13.0 ± 0.6 mmol/l of cells, P < 0.02), in ouabain-sensitive erythrocyte Na+ flux (from 17.8 ± 0.3 to 16.0 ± 0.4 mmol h−1 (1 of cells)−1, P < 0.01) and in ouabain-sensitive erythrocyte K+ flux (from 11.4 ± 0.2 to 10.4 ± 0.2 mmol h−1 (1 of cells)−1, P < 0.01). No change in blood pressure, erythrocyte cation concentration or Na+−K+ flux occurred when oestradiol and indomethacin were given together or when indomethacin was administered alone. 4. The hypertensive influence of oestradiol in normotensive rats was unaccompanied by any changes in erythrocyte K+ concentration, erythrocyte Na+ concentration and total, ouabain-sensitive and ouabain-resistant Na+−K+ flux. 5. The divergent changes in blood pressure noted in the two strains occurred despite comparable changes in plasma renin activity after oestradiol, with significant increases in plasma renin activity in normotensive rats (from 16.4 ± 4.2 to 28.4 ± 6.6 ng of angiotensin I h−1 ml−1, P < 0.05) and in spontaneously hypertensive rats (from 28.3 ± 2.7 to 39.5 ± 5.7 ng of angiotensin I h−1 ml−1, P < 0.01). The plasma renin activity in spontaneously hypertensive rats receiving oestradiol or indomethacin and oestradiol were similar with values of 39.5 ± 5.7 and 40.6 ± 5.7 ng of angiotensin I h−1 ml−1, respectively, but were significantly higher than that seen in control animals (28.3 ± 2.7 ng of angiotensin I h−1 ml−1, P < 0.01). Similarly, indomethacin alone induced a significant increase in plasma renin activity in spontaneously hypertensive rats to 35.8 ± 7.6 ng of angiotensin I h−1 ml−1 (P < 0.05). 6. The contrasting effects of oestradiol on blood pressure in the two rat strains occurred without any change in packed cell volume. Likewise, the changes in blood pressure in spontaneously hypertensive rats with either oestradiol alone or in combination with indomethacin occurred without any change in packed cell volume, although indomethacin alone resulted in a significant reduction in packed cell volume (from 30.9 ± 1.6 to 26.8 ± 2.0, P < 0.01). 7. The results suggest that the hypotensive action of oestradiol in spontaneously hypertensive rats might be mediated through its influence on erythrocyte cation concentration and/or the modulation of Na+−K+ flux either directly or via the action of prostanoids.

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