Effect of acute and chronic losartan therapy on active and inactive renin and active renin glycoforms*

1995 ◽  
Vol 8 (11) ◽  
pp. 1090-1098 ◽  
Author(s):  
John A. Opsahl ◽  
Michael R. Goldberg ◽  
Stephen A. Katz
Keyword(s):  
Active Renin ◽  
Inactive Renin

Ontogeny of neuronally released norepinephrine on renin secretion in sheep

1989 ◽  
Vol 257 (4) ◽  
pp. R765-R770 ◽  
Author(s):  
K. T. Nakamura ◽  
J. M. Klinkefus ◽  
F. G. Smith ◽  
T. Sato ◽  
J. E. Robillard
Keyword(s):  
Renin Secretion ◽  
Renal Nerves ◽  
Nerve Terminals ◽  
Norepinephrine Release ◽  
Fetal Sheep ◽  
Postnatal Maturation ◽  
Active Renin ◽  
Inactive Renin ◽  
Cortical Slices

The role of renal nerves and norepinephrine release on renin secretion during fetal and postnatal maturation has not been studied. Experiments were performed to determine the effect of veratridine, a substance known to promote norepinephrine release from nerve terminals, on active and inactive renin secretion from renal cortical slices of fetal (134-138 days gestation; term is 145 days), newborn (4-9 days of age), and adult nonpregnant sheep. Veratridine (10-300 microM) significantly increased active renin secretion and produced a small but nonsignificant rise in inactive renin secretion in all three groups of animals (P less than 0.05). The percent rise in active renin secretion during veratridine stimulation was similar among all groups. Veratridine-stimulated (300 microM) active renin secretion was antagonized by tetrodotoxin (0.5 and 5.0 microM) and DL-propranolol (1 microM) in fetal renal cortical slices. However, neither tetrodotoxin nor propranolol completely inhibited the stimulatory effect of veratridine on active renin secretion. These results suggest that 1) norepinephrine released from nerve terminals may regulate active renin secretion early during development; 2) the effect of veratridine on active renin secretion was similar in fetal, newborn, and adult sheep; 3) veratridine had no significant effect on inactive renin secretion; and 4) active renin secretion due to depolarization of nerve terminals in fetal sheep is dependent on activation of beta-adrenoceptors as it is in adults.

Two-Site Direct Immunoassay Specific for Active Renin

1992 ◽  
Vol 38 (10) ◽  
pp. 1959-1962 ◽  
Author(s):  
D Simon ◽  
D J Hartmann ◽  
G Badouaille ◽  
G Caillot ◽  
T T Guyenne ◽  
...  
Keyword(s):  
Magnetic Beads ◽  
Active Form ◽  
Plasma Renin ◽  
Active Plasma ◽  
Immunoradiometric Assay ◽  
Active Renin ◽  
Human Renin ◽  
Direct Immunoassay ◽  
Inactive Renin ◽  
Normotensive Subjects

Abstract A sensitive immunoradiometric assay, without an enzymatic step and specific for active human renin, was developed with use of two monoclonal antibodies (MAbs). In this assay system, the first MAb was coupled to magnetic beads (Magnogel); the second one, directed against the active form of the enzyme, was radiolabeled with 125I. The specificity of this assay was demonstrated in experiments measuring the active plasma renin concentration in the presence or absence of inactive renin. The assay, performed in two steps, was sensitive enough to detect 0.9 pg of renin per tube (3.5 ng/L). Intra- or interassay CVs were < 10%. Concentrations of active plasma renin measured in normotensive subjects were between 7 and 40 ng/L.

Acid-Activated Renin Responses to Hydrochlorothiazide, Propranolol and Indomethacin

1978 ◽  
Vol 55 (s4) ◽  
pp. 151s-153s ◽  
Author(s):  
J. K. McKenzie ◽  
E. Reisin
Keyword(s):  
Blood Pressure ◽  
Serum Potassium ◽  
Potassium Concentration ◽  
Hypertensive Patients ◽  
Serum Potassium Concentration ◽  
Active Renin ◽  
Serum Aldosterone ◽  
Low Salt ◽  
Inactive Renin ◽  
Marked Suppression

1. Six essential hypertensive patients (five with low renin) were treated in successive weeks with placebo; hydrochlorothiazide 100 mg (382 μmol)/day; hydrochlorothiazide and 50 mmol of sodium/day diet; hydrochlorothiazide, 50 mmol of sodium diet and propranolol 160 mg (544 μmol)/day; and hydrochlorothiazide, 50 mmol of sodium and indomethacin 100 mg (287 μmol)/day. 2. Although blood pressure remained unchanged and serum potassium fell on diuretic with or without low salt, there was a marked increase of active renin and a lesser increase of inactive renin, resulting in an increased proportion of active to total renin. 3. Propranolol decreased both active and inactive renin, but not significantly. 4. Indomethacin produced a marked suppression of active renin, a smaller reduction in inactive renin, and a reduction of the ratio of active to total renin almost to placebo values. 5. Blood pressure rose to control values on indomethacin despite the fall in renin whereas it fell with propranolol with little change in renin. 6. Serum aldosterone rose with stimulation but remained elevated despite effective renin suppression with indomethacin and continuing reduced serum potassium concentration.

Activators of Inactive Renin (‘Prorenin’) in Human Plasma: Their Connection with Kinin Formation, Coagulation and Fibrinolysis

1979 ◽  
Vol 57 (s5) ◽  
pp. 89s-92s ◽  
Author(s):  
F. H. M. Derkx ◽  
B. N. Bouma ◽  
H. L. Tan-Tjiong ◽  
M. A. D. H. Schalekamp
Keyword(s):  
Human Plasma ◽  
Hageman Factor ◽  
Active Renin ◽  
Normal Plasma ◽  
Inactive Renin ◽  
Fletcher Factor ◽  
Free Plasma ◽  
Renin Activation ◽  
Dependent Pathway ◽  
Proteolytic Pathways

1. Human plasma was treated at 4°C with acid, trypsin, plasmin, streptokinase, urokinase, active Hageman factor fragment (β-XIIa) and β-XIIa-activated plasma prekallikrein (Fletcher factor). The conversion of inactive into active renin (activation) was studied in normal plasma (n = 10), Hageman factor-deficient plasma (n = 2), Fletcher factor-deficient plasma (n = 1) and plasminogen-free plasma (n = 4). 2. In normal plasma inactive renin was activated at pH 7·5 after treatment at pH < 4·0; at pH 3·3 the results were the same as with trypsin. This was also the case in plasminogen-free plasma. In Hageman factor-deficient plasma and in Fletcher factor-deficient plasma, however, the quantities of renin that were activated after acidification were much smaller than with trypsin. The addition of physiological amounts of active kallikrein to pH 3·3-pretreated Hageman factor-deficient plasma caused complete activation of renin. In contrast, the addition of active Hageman factor fragment to pH 3·3-pretreated Fletcher factor-deficient plasma had little or no effect. 3. Plasmin, streptokinase-activated plasminogen and urokinase-activated plasminogen activated inactive renin in pH 4·0-pretreated normal plasma as well as in pH 4·0-pretreated Hageman factor-deficient plasma and Fletcher factor-deficient plasma. 4. It is concluded that inactive renin is activated by two separate proteolytic pathways: one pathway depends on both Hageman factor and plasma prekallikrein, and the other pathway depends on plasminogen. In the Hageman factor-dependent pathway plasma kallikrein and not Hageman factor is the major activator of inactive renin. It is assumed that pH 3·3-treatment of plasma destroys the major inhibitors of kallikrein and that pH 4·0-treatment destroys the major inhibitor of plasmin.

Effect of prostaglandin inhibition by indomethacin on plasma active and inactive renin concentration in men

1991 ◽  
Vol 69 (9) ◽  
pp. 1355-1359 ◽  
Author(s):  
P. Lijnen ◽  
J. Staessen ◽  
R. Fagard ◽  
A. Amery
Keyword(s):  
Plasma Concentrations ◽  
Work Load ◽  
Prostaglandin E ◽  
Active Renin ◽  
Prostaglandin F ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Inactive Renin ◽  
Exercise Induced ◽  
Total P ◽  
Rest And Exercise

The effect of inhibition of prostaglandin synthesis by indomethacin on active renin and on acid-activable inactive renin was studied in nine healthy, sodium-replete men, both at rest and exercise. These volunteers were investigated after pretreatment with placebo or indomethacin, 150 mg daily for 3 days. Indomethacin induced a decrease in active (p = 0.004), total (p < 0.001), and inactive (p = 0.02) renin at rest recumbent on average by 42, 19, and 8%, respectively, and at rest sitting on average by 45, 15, and 3%, respectively. Inhibition of prostaglandins with indomethacin reduced (p < 0.001) active and total renin at each level of work load but not (p = 0.32) inactive renin. However, the exercise-induced stimulation (p < 0.05) of active and total renin still occur during indomethacin. Indomethacin reduced (p < 0.001) at rest sitting and at maximal exercise the plasma concentrations of immunoreactive prostaglandins E2 by 50 and 54%, respectively, prostaglandin F2α by 36 and 39%, respectively, and 13,14-dihydro-15-keto-prostaglandin Fα by 38 and 60%, respectively. The urinary excretion of immunoreactive prostaglandin E2 and F2α was also reduced.Key words: indomethacin, prorenin, active renin, prostaglandins.

Active and Inactive Renin in Individual Juxtaglomerular Apparatuses

1980 ◽  
Vol 59 (s6) ◽  
pp. 35s-36s
Author(s):  
A. Gillies ◽  
T. Morgan ◽  
W. Fitzgibbon
Keyword(s):  
Salt Intake ◽  
Active Form ◽  
Juxtaglomerular Apparatus ◽  
Macula Densa ◽  
Active Renin ◽  
High Salt Intake ◽  
Before And After ◽  
Inactive Renin ◽  
Inhibitor Of Protein Synthesis

1. Renin was measured in individual juxtaglomerular apparatuses before and after acidification in vitro.. 2. Active renin increased with delivery of extra sodium by microperfusion to the macula densa and this increase was similar to that achieved with acidification. 3. In rats pretreated with an inhibitor of protein synthesis active renin increased when extra sodium was delivered to the macula densa. 4. Salt intake changed the amount of renin present in the juxtaglomerular apparatus. In rats on a high salt intake the total renin was low and was all in an active form.

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.

Active and inactive renin in primary and secondary adrenal insufficiency and during ACTH infusion

1983 ◽  
Vol 102 (2) ◽  
pp. 265-270
Author(s):  
Lutz Belkien ◽  
Petra Exner ◽  
Wolfgang Oelkers
Keyword(s):  
Plasma Renin ◽  
Renal Secretion ◽  
Young Males ◽  
Active Renin ◽  
Group I ◽  
Inactive Renin ◽  
Group Ii ◽  
Peripheral Activation ◽  
The Relationship ◽  
Stimulation Of

Abstract. Prolonged low-dose ACTH infusion leads to a transient stimulation of plasma renin activity (PRA) and angiotensin II. In part 1 of the present study (infusion of 10 IU of ACTH per day for 38 h into 6 normal young males), it was shown that the concentration of active renin (aPRC) increases in parallel to PRA. Thus, the rise in PRA is either due to net active renin secretion by the kidney or to increased conversion of inactive into active renin. Since the plasma concentration of inactive renin (iPRC) tended to rise rather than to fall during ACTH infusion, peripheral activation of inactive renin is probably not the cause of the rise in aPRC. Part 2 of the study consisted in the measurement of plasma ACTH, cortisol, PRA, aPRC and iPRC in 10 patients (group I) with primary adrenocortical insufficiency (8 Addisonians, 2 adrenalectomized Cushing's) and in 9 patients with hypopituitarism (group II) after short-term withdrawal of hydrocortisone substition therapy. ACTH was 1770 ± 390 pg/ml in the former and 20 ± 4 pg/ml in the latter group. PRA and aPRC were higher and the ratio iPRC:aPRC lower in group I than in group II. This might indicate stimulation of active renin formation by ACTH. However, it is unlikely that the higher aPRC levels in group I are due to increased peripheral activation of inactive renin, since the relationship between aPRC and the ratio iPRC:aPRC fell on the same curve in both groups. ACTH or an ACTH-dependent mechanism raises aPRC, probably by stimulating its renal secretion rather than by peripheral activation of inactive renin.

Selective Hypoaldosteronism due to Combined Defects of the Conversion from Inactive Renin to Active Renin and the Aldosterone Biosynthesis from Corticosterone

Nephron ◽  
2001 ◽  
Vol 88 (3) ◽  
pp. 247-253
Author(s):  
Shigeaki Muto ◽  
Youichi Akai ◽  
Shuichi Ono ◽  
Eiji Kusano ◽  
Yasushi Asano
Keyword(s):  
Active Renin ◽  
Inactive Renin ◽  
Combined Defects
Sign in / Sign up

Export Citation Format

Share Document