CIRCULATING LEVELS OF ACTIVE, TOTAL AND INACTIVE RENIN (PRORENIN), ANGIOTENSIN I AND ANGIOTENSINOGEN IN CARBON TETRACHLORIDE-TREATED RATS

1993 ◽  
Vol 20 (2) ◽  
pp. 83-88 ◽  
Author(s):  
Cristino Cruz ◽  
Maria Elena Ibarra-Rubio ◽  
José Pedraza-Chaverrí
Keyword(s):  
Carbon Tetrachloride ◽  
Angiotensin I ◽  
Inactive Renin ◽  
Circulating Levels

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.

Levels of active and inactive reninlike enzymes in plasma and reproductive tract of the pregnant wallaby

1994 ◽  
Vol 266 (4) ◽  
pp. R1353-R1358
Author(s):  
E. R. Lumbers ◽  
R. I. Menzies ◽  
K. J. Gibson ◽  
C. H. Tyndale-Biscoe
Keyword(s):  
Reproductive Tract ◽  
Maternal Plasma ◽  
Yolk Sac ◽  
Female Reproductive Tract ◽  
Fetal Membranes ◽  
Low Permeability ◽  
Angiotensin I ◽  
Total Acid ◽  
Plasma Active Renin ◽  
Inactive Renin

Active and total (acid-activated) levels of a reninlike enzyme (hereafter called renin) were measured in plasma, tissues, and yolk sac fluid of pregnant and postpartum wallabies. Plasma active renin generated angiotensin I (ANG I) from sheep angiotensinogen at 14 +/- 1.3 (SE) ng.ml-1.h-1, whereas acid-activated renin generated ANG I at 33.3 +/- 2.5 ng.ml-1.h-1, i.e., 44.2 +/- 3.7% of renin in plasma was active, and 58 +/- 3.7% was inactive. Inactive renin levels were highest in pregnant animals (P = 0.05). Uterine renin was mainly inactive (95%); levels were 5.1 +/- 1.1 times plasma levels. The levels of renin in nonpregnant uteri were the same as those in pregnant uteri from the same animals. Uterine renin levels did not change with gestation. Pooled acid-activated yolk sac fluid generated ANG I at low rates (0.7 and 1.6 ng.ml-1.h-1); the acid-activated supernatant of a homogenate of pooled fetal membranes generated ANG I at 15 ng.g wet wt-1.h-1. Yolk sac fluid was strikingly different in electrolyte composition from maternal plasma. Its lower osmolality suggests that the membranes separating it from maternal plasma have a low permeability to water. Thus, although eutherian and marsupial mammals diverged 136-164 million years ago, the wallaby, like many eutherian mammals, has inactive renin in blood, in the female reproductive tract, and in fetal membranes.

Angiotensin I-Converting Enzyme Activity in Rats with Carbon Tetrachloride-Induced Acute Renal Failure

Renal Failure ◽  
1993 ◽  
Vol 15 (1) ◽  
pp. 19-26 ◽  
Author(s):  
Jose Pedraza-chaverri ◽  
Cristino Cruz ◽  
Rogelio Hernandez-pando ◽  
Thalia Santana ◽  
Ana Elena Arevalo ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Enzyme Activity ◽  
Carbon Tetrachloride ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Angiotensin I Converting Enzyme

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.

EFFECT OF INHIBITION OF CONVERTING ENZYME ON INACTIVE RENIN IN THE CIRCULATION OF SALT-REPLETE AND SALT-DEPLETE NORMAL SUBJECTS

1980 ◽  
Vol 86 (2) ◽  
pp. 329-335 ◽  
Author(s):  
J. A. MILLAR ◽  
M. T. HAMMAT ◽  
C. I. JOHNSTON
Keyword(s):  
Angiotensin Ii ◽  
Normal Subjects ◽  
Inhibitory Influence ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Active Inhibitor ◽  
Active Renin ◽  
Angiotensin I Converting Enzyme ◽  
Inactive Renin ◽  
Orally Active

Angiotensin II exerts an inhibitory influence on active renin release from the kidney. To assess a possible role for angiotensin II in the release of inactive renin, levels in the circulation were measured before and at regular intervals after the administration of captopril, an orally active inhibitor of angiotensin I-converting enzyme, to 12 salt-replete and six salt-deplete normal subjects. Concurrent measurements of active renin, angiotensin I and angiotensin II were also performed. Basal inactive renin in the salt-deplete group was increased compared with the salt-replete subjects, but inactive renin remained constant in both groups after treatment with captopril. There were significant increases in concentrations of both active renin and angiotensin I after treatment with captopril in all subjects and corresponding decreases in angiotensin II. These results suggested that angiotensin II does not influence the release of inactive renin, in contrast with its role in the release of active renin.

scholarly journals Sacubitril/valsartan (LCZ696) Significantly Reduces Aldosterone and Increases cGMP Circulating Levels in a Canine Model of RAAS Activation

2018 ◽  
Author(s):  
Jonathan P Mochel ◽  
Chi Hse Teng ◽  
Mathieu Peyrou ◽  
Jerome Giraudel ◽  
Meindert Danhof ◽  
...  
Keyword(s):  
Heart Failure ◽  
Systemic Exposure ◽  
Plasma Renin ◽  
Canine Model ◽  
Angiotensin Receptors ◽  
Angiotensin I ◽  
Once Daily ◽  
Salt Diet ◽  
Low Salt ◽  
Circulating Levels

AbstractSimultaneous blockade of angiotensin receptors and enhancement of natriuretic peptides (NP) by the first-in-class angiotensin receptor neprilysin (NEP) inhibitor sacubitril/valsartan constitutes an effective approach to treating heart failure. This study examined the effects of sacubitril/valsartan (225 and 675mg/day) vs. placebo, sacubitril (360mg/day), valsartan (900mg/day), and benazepril (5mg/day) on the dynamics of the renin-angiotensin-aldosterone system (RAAS) and the NP system in dogs. Beagle dogs (n=18) were fed a low-salt diet (0.05% Na) for 15 days to model RAAS activation observed in clinical heart failure. Drugs were administered once daily during the last 10 days, while the effects on the RAAS and NPs were assessed on days 1, 5, and 10. Steady-state pharmacokinetics of the test agents were evaluated on day 5. Compared with placebo, sacubitril/valsartan (675mg) substantially increased cGMP circulating levels, while benazepril and valsartan showed no effect. Additionally, sacubitril/valsartan (675mg) and valsartan significantly increased plasma renin activity, angiotensin I and angiotensin II concentrations. Finally, sacubitril/valsartan (both doses), and valsartan significantly decreased plasma aldosterone vs. placebo. Systemic exposure to valsartan following sacubitril/valsartan 675mg administration was similar to that observed with valsartan 900mg administration alone. Sacubitril/valsartan favorably modulates the dynamics of the renin and NP cascades through complementary NEP and RAAS inhibition.

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.

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