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.

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.

Hypertension in Dahl salt-sensitive rats: biochemical and immunohistochemical studies

1992 ◽  
Vol 83 (1) ◽  
pp. 13-22 ◽  
Author(s):  
J. Bouhnik ◽  
J. P. Richoux ◽  
H. Huang ◽  
F. Savoie ◽  
T. Baussant ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
High Salt ◽  
Renin Activity ◽  
Deficient Diet ◽  
High Salt Diet ◽  
Salt Diet ◽  
Plasma Angiotensin

1. The renin-angiotensin and kinin-kallikrein systems of Dahl salt-sensitive and salt-resistant rats fed diets with different salt contents were analysed using biochemical and immunocytochemical techniques. 2. Blood pressure increased by 45% in salt-sensitive rats only, after 4 weeks on a high-salt diet. The plasma renin activity and plasma angiotensin II concentration remained at the same levels in salt-sensitive rats on the high-salt diet as on the normal salt diet, whereas the plasma renin activity and plasma angiotensin II concentration of salt-resistant rats fed the high-salt diet were lower. The plasma renin activity and the plasma angiotensin II concentration were elevated in both salt-resistant and salt-sensitive rats fed the salt-deficient diet but were much more elevated in salt-resistant than in salt-sensitive rats. 3. The kidney immunocytochemical data paralleled the data on plasma parameters. Salt-sensitive rats had fewer renin positive juxtaglomerular apparatuses than salt-resistant rats on the normal diet, and the increase on the sodium-deficient diet was also smaller in salt-sensitive rats. Salt-sensitive rats fed the high-salt diet and the standard diet had almost no angiotensin II immunoreactivity compared with the salt-resistant rats on the same diets. 4. The total renal kallikrein content of salt-sensitive rats was lower than that of salt-resistant rats on all three diets, as was the amount of kallikrein excreted in the urine on the standard and the high-salt diets. The differences resulted from a reduction in active kallikrein. The increase in kallikrein in salt-sensitive and salt-resistant rats on the salt-deficient diet was not significantly different. 5. There were similar changes in immunopositive kallikrein in the kidneys of salt-sensitive and salt-resistant rats with diet, with a large increase in kallikrein biosynthesis on the low-salt diet. The plasma concentration of high-molecular-mass kininogen was not significantly different in salt-sensitive and salt-resistant rats, but there was a significant increase in T-kininogen in salt-sensitive rats fed the high-salt diet. 6. In conclusion, the absence of decreases in the plasma renin activity and the plasma angiotensin II concentration in salt-sensitive rats fed the high-salt diet might partially explain the increase in blood pressure.

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.

Effect of aldosterone on vascular angiotensin II receptors in the rat

1985 ◽  
Vol 63 (12) ◽  
pp. 1522-1527 ◽  
Author(s):  
Ernesto L. Schiffrin ◽  
Douglas J. Franks ◽  
Jolanta Gutkowska
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Binding Sites ◽  
Mesenteric Artery ◽  
Plasma Renin ◽  
Renin Activity ◽  
Angiotensin Ii Receptors ◽  
Rat Mesenteric Artery ◽  
Plasma Angiotensin ◽  
Dose Dependent Fashion

The effect of aldosterone on the density and affinity of binding sites for 125I-labelled angiotensin II was investigated in a particulate fraction prepared from the rat mesenteric arteriolar arcades. The infusion of aldosterone 6.6 μg/h intraperitoneally via Alzet osmotic minipumps for 6 d produced an increase in the density of binding sites for 125I-labelled angiotensin II without change in affinity. After sodium depletion, mesenteric artery angiotensin II receptors were down-regulated as expected. An increase in the number of binding sites could be found when aldosterone was infused into sodium-depleted rats with no change in the elevated plasma renin activity. The intraperitoneal infusion of angiotensin II (200 ng ∙ kg−1 ∙ min−1 for 6 d) simultaneously with aldosterone resulted in down-regulation of vascular angiotensin II receptors, whereas after intravenous angiotensin II infusion (at 60 ng ∙ kg−1 ∙ min−1) the density of angiotensin II binding sites rose with aldosterone infusion. Plasma renin activity (PRA) was reduced and plasma angiotensin II increased in a dose-dependent fashion after angiotensin II infusion. An aldosterone concentration of 3 ng/mL for 18 h produced an increase in the number of angiotensin II binding sites in rat mesenteric artery smooth muscle cells in culture. We conclude that increased plasma aldosterone may result in up-regulation of vascular angiotensin II receptors independently of changes in plasma renin activity, and may in certain physiological states effectively antagonize the down-regulating action of angiotensin II.

Plasma Renin Activity, Plasma Angiotensin and Plasma and Urinary Electrolytes in Normal and Toxaemic Pregnancy, Including a Prospective Study

1973 ◽  
Vol 45 (1) ◽  
pp. 115-127 ◽  
Author(s):  
R. D. Gordon ◽  
E. M. Symonds ◽  
E. G. Wilmshurst ◽  
C. G. K. Pawsey
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Prospective Study ◽  
Plasma Renin ◽  
Late Pregnancy ◽  
Normal Pregnancy ◽  
Renin Activity ◽  
Creatinine Ratio ◽  
Plasma Angiotensin ◽  
A Prospective Study

1. In a prospective study involving fifty-six women, measurements of body weight, urinary creatinine, sodium and potassium and plasma sodium, potassium and renin activity were made in mid-pregnancy and at 36 weeks. The effect of sodium restriction and sodium loading on these measurements was assessed in mid-pregnancy. 2. Mean plasma renin activity was significantly higher throughout pregnancy than the normal non-pregnant mean level. It was lower at 36 weeks than in mid-pregnancy in those whose pregnancy was normal but not in those who developed toxaemia of pregnancy between 38 and 40 weeks. In mid-pregnancy in both groups sodium depletion was significantly elevated but sodium loading did not significantly depress plasma renin activity. 3. The urinary potassium/creatinine ratio in mid-pregnancy and urinary sodium/creatinine ratio at 36 weeks were lower in those who subsequently developed toxaemia, raising the possibility of a functional renal lesion which antedates the morphologically recognizable lesion of late pregnancy. 4. In a second study involving sixty-six different women plasma angiotensin II levels between 6 and 40 weeks of pregnancy were mostly above the normal range, and highest levels were observed between 21 and 30 weeks. The plasma angiotensin II levels in six women with established toxaemia of pregnancy were not significantly different from the levels in nine women with normal pregnancy of the same duration. 5. While the renal glomerular lesion is presumably the major determinant in the development of toxaemia, the heightened activity of the renin-angiotensin-aldosterone system which is appropriate to normal pregnancy is an aggravating factor in established toxaemia, and may predispose to its development in some patients by failing to decline in late pregnancy.

Theoretical approaches to estimation of plasma renin activity: a review and some original observations.

1976 ◽  
Vol 22 (5) ◽  
pp. 583-593 ◽  
Author(s):  
S Oparil
Keyword(s):  
Plasma Renin Activity ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Renin Activity ◽  
Clear Understanding ◽  
Angiotensin I ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Theoretical Approaches

Abstract Performance of accurrate, reproducible, and interpretable assays for plasma renin activity and other components of the renin/angiotensin system in the clinical setting requires a clear understanding of the various reactions in the renin/angiotensin cascade and the nature of their interactions. Plasma renin activity, the rate of angiotensin generations from plasma incubated in vitro, is the most commonly used clinical index of function in the renin/angiotensin system. Renin activity is measured by radioimmunoassay of angiotensin I generated in vitro under carefully controlled conditions. The value obtained for plasma renin activity depends on pH and duration of incubation and on the method used to protect the angiotensin I generated. We recommend incubation at neutral pH in buffered plasma for three hours in the presence of either ethylenediaminetetraacetate + 8-hydroxyquinolone + dimercaprol or ethylenediaminetetraacetate + phenylmethylsulfonylfluoride. Addition of a standard preparation of human renin to the plasma incubation step of the renin activity assay serves the dual purpose of permitting measurement of renin activity and furnishing an internal standard for comparison of assay procedures. The many variables among renin assay methods can be cancelled by referring to a common internal renin standard.

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