Enzymatic Activity of Renin in Plasma of Normal and Uraemic Subjects

1984 ◽  
Vol 67 (3) ◽  
pp. 365-368 ◽  
Author(s):  
Theodore A. Kotchen ◽  
Tam T. Guyenne ◽  
Pierre Corvol ◽  
Joel Menard
Keyword(s):  
Renal Failure ◽  
Enzymatic Activity ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Renin Activity ◽  
Angiotensin I ◽  
Renin Substrate ◽  
Inactive Renin ◽  
Substrate Concentrations

1. Plasma renin reactivity (PRR) is the rate of angiotensin I production after addition of renin to plasma, minus endogenous renin activity. PRR is increased in plasma of patients with renal failure compared with that of normal subjects. The present study was carried out to determine if increased PRR in uraemic plasma is related to differences of endogenous active or inactive renin, endogenous renin substrate, or pH of the incubation in vitro. 2. PRR in plasma of ten uraemic patients was greater (P<0.02) than that in plasma of ten normal subjects in incubations carried out at pH 7.4 and 5.7. 3. Increased PRR was not accounted for by differences of endogenous active and inactive renin activity. 4. After addition of renin, renin concentration (measured by direct radioimmunoassay) did not differ in normal and uraemic plasma. 5. Renin substrate concentration, measured both indirectly and by direct radioimmunoassay, also did not differ in normal and uraemic plasma. 6. Increased PRR in uraemic plasma is not related to alterations of renin or renin substrate concentrations. These observations are consistent with our earlier hypothesis that there is a deficiency of a renin inhibitor in uraemic plasma.

Increased enzymatic activity of renin and hyperlipidemia

1981 ◽  
Vol 240 (1) ◽  
pp. E60-E64 ◽  
Author(s):  
T. A. Kotchen ◽  
R. T. Talwalkar
Keyword(s):  
Renal Failure ◽  
Enzymatic Activity ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Renin Inhibitor ◽  
Renin Substrate ◽  
Control Subjects ◽  
Endogenous Substrate ◽  
Uremic Patients

We have previously reported that the in vitro enzymatic activity of exogenous renin, plasma renin reactivity (PRR), is increased in plasma of patients with chronic renal failure, possibly due to the deficiency of a renin inhibitor. To determine whether increases PRR is related to renal failure per se or to hyperlipidemia, PRR was measured in 10 control subjects, 10 patients with renal failure, and 10 hyperlipidemic patients with normal renal function. Compared to that in control subjects (52.6 ng angiotensin I generated per ml/h +/- 3.8 SE) PRR was increased (P < 0.05) in plasma of uremic patients (65.1 +/- 4.3) and hyperlipidemic patients (71.4 +/- 10.7). Renin substrate concentration did not differ among groups, and after denaturation of endogenous substrate by acidification of plasma, PRR was still increased. A "protein-free" extract of plasma from normal subjects inhibited renin, whereas little or no inhibition occurred with a comparable extract from uremic patients and hyperlipidemic patients. Thus, alterations in lipid metabolism may account for the increased enzymatic activity of renin in uremic plasma. Increased PRR may be related to the deficiency of a normally occurring renin inhibitor.

Measurement of inactive renin in normal, nephrectomized, and adrenalectomized rats

1991 ◽  
Vol 69 (9) ◽  
pp. 1381-1384 ◽  
Author(s):  
Knud Poulsen ◽  
Arne Høj Nielsen ◽  
Arne Johannessen
Keyword(s):  
Animal Model ◽  
Exchange Resin ◽  
Cation Exchange Resin ◽  
Plasma Renin ◽  
Rat Plasma ◽  
Angiotensin I ◽  
Renin Substrate ◽  
Suitable Animal Model ◽  
Inactive Renin ◽  
Adrenalectomized Rats

In a new method for measurement of inactive rat plasma renin, the trypsin generated angiotensin I immunoreactive material, which was HPLC characterized as similar to tetradecapeptide renin substrate, is removed by a cation exchange resin before the renin incubation step. The method also corrects for trypsin destruction of endogenous angiotensinogen by the addition of exogenous angiotensinogen. When measured with this method inactive renin in rat plasma decreased after nephrectomy and increased after adrenalectomy. This is in accordance with findings in humans. A sexual dimorphism of prorenin (inactive renin) in rat plasma, similar to that reported in humans and mice, was demonstrated. Thus, inactive renin in the rat is no exception among species, and the rat might be a suitable animal model for further studies dealing with the physiology of prorenin in plasma and tissues.Key words: angiotensinogen, inactive renin, renin.

Does heparin inhibit renin activity?

1991 ◽  
Vol 69 (9) ◽  
pp. 1360-1363 ◽  
Author(s):  
Masato Matsunaga ◽  
Yoko Yamanaka ◽  
Noriko Nagano ◽  
Yuki Iwasaki ◽  
Yumi Saito ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Substrate ◽  
Significant Difference ◽  
Inactive Renin

Although heparin was reported in the 1960s to inhibit renin activity, this has not always been confirmed by other investigators. Hence, we re-examined whether heparin really inhibits renin or not. Renin activities were determined by radioimmunoassay of angiotensin I generated at pH 7.4. (i) No significant difference was found between the two kinds of plasma samples obtained with heparin and with EDTA as anticoagulant, in ARC (renin activity with addition of sheep renin substrate), TRC (ARC after activation of inactive renin by trypsin), or PRA (plasma renin activity without additional substrate), (ii) Even in higher concentrations of heparin up to 500 U/mL, neither PRA, ARC, nor TRC of plasma was affected significantly. (iii) Heparin, in concentrations up to 500 U/mL, exerted no significant effect on TRC of the media of human vascular smooth muscle cell culture. In conclusion, heparin does not exert any significant inhibitory effect on human renin nor does it affect activation of inactive renin by trypsin in the range of concentration of practical use, under the conditions employed in this study.Key words: plasma renin, tissue renin, inactive renin, vascular smooth muscle cell, trypsin.

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.

BIOLOGICAL SIGNIFICANCE OF ACTIVE AND INACTIVE RENIN IN MAN

1980 ◽  
Vol 85 (1) ◽  
pp. 137-143 ◽  
Author(s):  
P. LIJNEN ◽  
A. AMERY ◽  
R. FAGARD ◽  
L. VERSCHUEREN
Keyword(s):  
Plasma Concentrations ◽  
Biological Significance ◽  
Plasma Renin ◽  
Angiotensin I ◽  
Vitro Assay ◽  
Arterial Blood ◽  
Inactive Renin ◽  
Change In Mean

SUMMARY The biological significance of active and inactive renin was investigated by comparison of an in-vitro assay of active, total and inactive plasma renin concentration (PRC), plasma renin activity (PRA) and plasma concentrations of angiotensin I and II with an in-vivo change in mean arterial blood pressure (MAP) produced by antagonism of angiotensin with treatment with saralasin and by blockade of angiotensin-converting enzyme by treatment with captopril. A significant relationship between the changes in MAP during treatment with saralasin and captopril with the pretreatment levels of PRA, active and total PRC and angiotensin II were found; while the pre-existing level of inactive renin was not a predictor for the hypotensive effect of saralasin and captopril. During treatment with saralasin and captopril significant increases in PRA, plasma angiotensin I concentration and total and active PRC were found and no change in inactive PRC was observed.

Characterization of Aggression-Provoked Renin from An Unknown Source in Male Mice

1981 ◽  
Vol 61 (4) ◽  
pp. 373-378 ◽  
Author(s):  
K. Poulsen ◽  
E. B. Pedersen
Keyword(s):  
Enzymatic Activity ◽  
Control Level ◽  
Plasma Renin ◽  
Fold Increase ◽  
Male Mice ◽  
Angiotensin I ◽  
Renin Substrate ◽  
Specific Enzymatic Activity ◽  
Aspartate Proteinase

1. In male mice without kidneys and submaxillary, as well as sublingual, glands aggressive behaviour causes a vast release of renin [J. Bing & K. Poulsen (1979) Acta Physiologica Scandinavica, 107, 251–256]. 2. This resulted in about an 800-fold increase in plasma renin concentration from the control level of 0.52 (range 0.15-0.8) Goldblatt unit (G.U.) × 10−3/ml to 430 (range 300–500) G.U. × 10−3/ml after aggression. 3. The aggression-provoked renin fulfil all the criteria so far studied for being active renin, identical with normal mouse plasma renin and pure submaxillary mouse renin. 4. It generates angiotensin I with renin substrate and Km (1.2 μmol/l) is the same. It is neutralized by pepstatin but not by inhibitors of metallo-, thiol and serine proteinases, indicating that it is an aspartate proteinase (acidic proteinase). 5. It is a 40 000-mol.wt. renin, which has full enzymatic activity with a specific enzymatic activity of 0.32 G.U./μg, identical with that of normal plasma renin. 6. Its enzymatic activity is neutralized by a specific antibody against pure submaxillary renin. It is measurable in the direct renin radioimmunoassay with a dilution curve which parallels that of the standards. It demonstrates complete antigenic identity with pure submaxillary renin in crossed immunoelectrophoresis. 7. Its origin is unknown.

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.

Control of Renin Secretion in Vivo and in Vitro in Rats: Arguments in Favour of a Precursor Form of Renin and of a Role of a Microtubular System

1976 ◽  
Vol 51 (s3) ◽  
pp. 93s-95s ◽  
Author(s):  
F. Banichahi ◽  
A. Capponi ◽  
C. Pricam ◽  
C. De Senarclens ◽  
M. B. Vallotton
Keyword(s):  
Endoplasmic Reticulum ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Juxtaglomerular Apparatus ◽  
Granular Endoplasmic Reticulum ◽  
Renin Activity ◽  
Renin Substrate ◽  
Salt Depletion

1. The morphology of the juxtaglomerular apparatus, plasma renin activity, plasma renin substrate and renal renin have been studied in rats after maximal stimulation by bilateral adrenalectomy and salt depletion, and also after blocking this stimulation by deoxycorticosterone and salt load. 2. After stimulation the juxtaglomerular apparatus showed a well-developed granular endoplasmic reticulum and a low secretory granule content. Plasma renin activity was markedly elevated and plasma renin substrate was low. After blockade numerous specific granules with crystalline structures were seen and the granular endoplasmic reticulum was less developed. Plasma renin activity was now low and plasma renin substrate elevated. 3. After prior acidification of the kidney extract a significant increase of renal renin was observed in both conditions but was greater in the second group at the time when large numbers of young granules containing crystalline material were seen. 4. Kidney slices from the adrenalectomized salt-depleted rats released more renin than control slices. Vincristine did not affect this release, but inhibited release from slices stimulated by isoprenaline.

Sign in / Sign up

Export Citation Format

Share Document