Renin Secretion by the Human Kidney

1978 ◽  
Vol 55 (s4) ◽  
pp. 147s-149s
Author(s):  
W. H. Birkenhäger ◽  
P. W. De Leeuw ◽  
H. E. Falke ◽  
G. A. W. Van Soest
Keyword(s):  
Blood Flow ◽  
Active Form ◽  
Human Kidney ◽  
Blood Samples ◽  
Active Renin ◽  
Intrarenal Blood Flow ◽  
Inactive Renin ◽  
Propranolol Treatment ◽  
Xenon Washout

1. 20 subjects with uncomplicated essential hypertension were studied, 10 of whom were on propranolol treatment. Several blood samples for determination of total and active renin were drawn simultaneously from the renal artery and vein after angiographic studies. 2. In all patients renal blood flow was measured by Hippuran-clearance at the time of blood sampling. Intrarenal blood flow was assessed by xenon-washout. 3. The results indicate that under basal conditions renin is secreted mainly in the active form, although secretion of inactive renin does occur. During propranolol treatment there is a tendency for secretion of active renin to be reduced.

Noradrenaline Secretion by the Human Kidney

1978 ◽  
Vol 55 (s4) ◽  
pp. 85s-87s ◽  
Author(s):  
P. W. De Leeuw ◽  
H. E. Falke ◽  
R. Punt ◽  
W. H. Birkenhäger
Keyword(s):  
Blood Flow ◽  
Human Kidney ◽  
Treated Group ◽  
Blood Samples ◽  
Hypertensive Patients ◽  
Active Renin ◽  
Noradrenaline Secretion ◽  
Propranolol Treatment ◽  
Arteriovenous Difference ◽  
Xenon Washout

1. In 20 subjects with uncomplicated essential hypertension, 10 of whom were on propranolol treatment, several blood samples were drawn simultaneously from the renal artery and vein after angiographic studies. In these samples we determined concentrations of noradrenaline, active renin, aldosterone and cortisol. 2. Renal blood flow was measured in all patients by Hippuran-clearance and xenon-washout. 3. Despite marked variations in the arteriovenous difference of noradrenaline, it was apparent in both groups that the kidney is able to release noradrenaline. 4. In the propranolol-treated group noradrenaline secretion by the kidney was enhanced when compared with untreated hypertensive patients.

Evidence for Activation of Circulating Inactive Renin by the Human Kidney

1979 ◽  
Vol 56 (2) ◽  
pp. 115-120 ◽  
Author(s):  
F. H. M. Derkx ◽  
G. J. Wenting ◽  
A. J. Man In't Veld ◽  
R. P. Verhoeven ◽  
M. A. D. H. Schalekamp
Keyword(s):  
Renal Vein ◽  
Human Kidney ◽  
Activation Process ◽  
Peripheral Vein ◽  
Active Renin ◽  
A Value ◽  
Before And After ◽  
Inactive Renin ◽  
Propranolol Treatment ◽  
Stimulation Of

1. In eight patients with essential hypertension (EHT) and six patients with renovascular hypertension (RVHT) peripheral venous enzymatically active and inactive renin values were followed after acute stimulation of renin release by the vasodilating agent diazoxide (300 mg intravenously). Active renin rose during the first hour after diazoxide and remained high during the following 15 h, but inactive renin fell during the first hour and rose thereafter. Peripheral venous active and inactive renin were not different from arterial values both before and after diazoxide. 2. Sixteen patients with EHT received propranolol, 80 mg, four times a day. Six of them had a first injection of diazoxide the day before propranolol was started and a second one after 10–14 days of propranolol treatment. Peripheral vein active renin was lowered by propranolol, but inactive renin was raised. Both the diazoxide-induced rapid rise of active renin and the fall of inactive renin observed in untreated patients were absent during treatment with propranolol. 3. In four patients with EHT and seven patients with RVHT renal vein sampling was performed before and 30 min after diazoxide. Increased release of active renin from kidneys that were not markedly contracted was associated with a fall of the renal vein to peripheral vein ratio of inactive renin to a value less than one. 4. It is concluded that under certain circumstances stimulated release of active renin is associated with removal of inactive renin from the circulation by the kidney. This may in fact be due to intrarenal transformation of circulating inactive renin into its active counterpart. The findings suggest that a β-adrenoreceptor might be involved in this activation process.

Measurement of Intrarenal Blood-Flow Distribution in the Rabbit Using Radioactive Microspheres

1975 ◽  
Vol 48 (1) ◽  
pp. 51-60 ◽  
Author(s):  
D. J. Warren ◽  
J. G. G. Ledingham
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Renal Cortex ◽  
Flow Distribution ◽  
Rabbit Kidney ◽  
Radioactive Microspheres ◽  
Injection Dose ◽  
Intrarenal Blood Flow ◽  
Total Renal Blood Flow

1. Total renal blood flow and its distribution within the renal cortex of the conscious rabbit were studied with radioactive microspheres of 15 and 25 μm diameter. 2. The reliability of the microsphere technique was influenced by microsphere diameter and number (dose). The optimum microsphere diameter for determination of flow distribution in the rabbit kidney was 15 μm and dose 100–150 000 spheres. 3. Spheres of 15 μm nominal diameter were randomly distributed within the renal cortex of adult rabbits. The larger spheres in batches nominally 15 μm in diameter in young rabbits and 25 μm diameter in adult rabbits were preferentially distributed to the superficial cortex. 4. In adult rabbits 15 μm diameter spheres lodged in glomerular capillaries. Larger spheres occasionally lodged in interlobular arteries causing intrarenal haemorrhage. 5. Microspheres of 15 μm caused a decrease in renal clearance of creatinine and of p-aminohippurate when the total injection dose was about 200 000 spheres. These effects were greater when the injection dose was increased to 500 000 spheres. 6. The reduction in total renal blood flow observed with large doses of spheres largely reflected decreased outer cortical flow, as measured by a second injection of spheres, and confirmed by a decrease in p-aminohippurate extraction. 7. The reproducibility of multiple injection studies was limited by these intrarenal effects of microspheres. 8. Total renal blood flow measured in six rabbits in acute experiments by the microsphere technique was 107 ± 12 (mean±sd) ml/min and by p-aminohippurate clearance was 100 ± 10 ml/min. 9. Total renal blood flow in twelve conscious, chronically instrumented rabbits was 125 ± 11 ml/min, of which 92 ± 6 ml/min was distributed to the superficial cortex and 33 ± 4 ml/min to the deep cortex.

scholarly journals Intrarenal Blood Flow Distribution (IRBF) in the Puppy Using Xenon Washout and Microspheres

1970 ◽  
Vol 4 (5) ◽  
pp. 446-446
Author(s):  
Pedro A Jose ◽  
Alexander G Logan ◽  
Gilbert M Eisner ◽  
Lawrence M Slotkoff ◽  
Charles E Hollerman ◽  
...  
Keyword(s):  
Blood Flow ◽  
Flow Distribution ◽  
Blood Flow Distribution ◽  
Intrarenal Blood Flow ◽  
Xenon Washout

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.

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.

Biochemical and immunological differences between plasma inactive renin from normal and nephrectomized rats

1991 ◽  
Vol 69 (9) ◽  
pp. 1350-1354 ◽  
Author(s):  
Shokei Kim ◽  
Masayuki Hosoi ◽  
Kiichiro Nakajima ◽  
Kenjiro Yamamoto
Keyword(s):  
Molecular Weight ◽  
Hplc Analysis ◽  
Rat Plasma ◽  
The Other ◽  
Trypsin Treatment ◽  
Angiotensin I ◽  
Active Renin ◽  
Normal Rat ◽  
Inactive Renin

Using immunological techniques, we have demonstrated that about half the trypsin-activatable renin in normal rat plasma is prorenin, while the other is not, and that inactive renin in nephrectomized rat plasma is not prorenin. In the present study, the trypsin-induced angiotensin I generating activity not related to prorenin from normal rat plasma disappeared after HPLC on G3000SW. HPLC analysis of trypsin-treated plasma showed the generation of active renin by trypsin for normal rat plasma, while it did not for nephrectomized rat plasma. These results indicate that trypsin treatment of crude plasma results in the generation of angiotensin I generating activity not due to prorenin, as well as activation of prorenin. HPLC on G3000SW is a useful tool for the determination of plasma prorenin.Key words: prorenin, antibody against prorenin prosegment, trypsin treatment, molecular weight, nephrectomy.

Generation of Inactive Renin in Vitro and in Vivo: Reversible Inactivation of the Active Plasma Enzyme in Rats

1982 ◽  
Vol 63 (s8) ◽  
pp. 171s-174s ◽  
Author(s):  
Jack D. Barrett ◽  
Peter Eggena ◽  
Mohinder P. Sambhi
Keyword(s):  
Active Form ◽  
Renin Angiotensin System ◽  
Active Plasma ◽  
Reversible Inactivation ◽  
Active Renin ◽  
Plasma Enzyme ◽  
Inactive Renin ◽  
Rate Of Decline

1. Active and total (trypsin treatment) plasma renins were measured in normal Wistar rats and in rats in which the renin-angiotensin system was stimulated by ether anaesthesia. 2. After incubation of normal plasma in vitro in the absence of angiotensinase inhibitors, active renin declined. This decline was shown to be due to the conversion of active renin into an inactive form, which could be re-activated by trypsin. 3. In plasma from renin-stimulated rats, the rate of decline of active renin in vitro was accelerated; however, the relative amount of inactive renin generated was decreased. 4. Ligation of the kidneys of the ether-anaesthetized animal resulted in a build-up in vivo of inactive renin concomitant with the decline of active renin. 5. These data demonstrate the conversion of active into inactive renin in vitro and indicate that inactive renin can also be generated in vivo from the active form of the enzyme. 6. Multiple forms of inactive renin may exist; some may be true ‘prorenins’ (renin zymogens) produced in the kidney, and others may result from post-biosynthetic modifications of the active plasma enzyme.

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