Evidence that ‘Inactive’ Renin is Produced outside the Kidney of the Rat

1977 ◽  
Vol 53 (2) ◽  
pp. 189-191
Author(s):  
R. Vandongen ◽  
Marianne Poessée ◽  
K. D. Strang ◽  
W. H. Birkenhäger
Keyword(s):  
Rat Kidney ◽  
Active Form ◽  
Peripheral Plasma ◽  
Perfused Rat Kidney ◽  
Before And After ◽  
Inactive Renin ◽  
Anephric Patients

1. Inactive renin, which can be converted into an active form by acidification to pH 3·3, represents 4–63% of the total renin in rat peripheral plasma. 2. No inactive component could be found in the blood-free venous effluent of the perfused rat kidney before and after stimulation with isoprenaline. 3. This suggests a possible extrarenal source for inactive renin and may explain the presence of this component in anephric patients.

A Comparison of Multiple Forms of Renin in Rat Renal Perfusate with those in Renal Extract

1980 ◽  
Vol 59 (s6) ◽  
pp. 37s-40s ◽  
Author(s):  
Haruyuki Nakane ◽  
Yoko Nakane ◽  
Jiro Misumi ◽  
Takao Saruta ◽  
Pierre Corvol ◽  
...  
Keyword(s):  
Molecular Weight ◽  
High Molecular Weight ◽  
Rat Kidney ◽  
Relative Proportion ◽  
Active Form ◽  
Low Molecular Weight ◽  
Multiple Forms ◽  
Isoelectric Points ◽  
Perfused Rat Kidney ◽  
Inactive Renin

1. Physicochemical properties of renin secreted by isolated perfused rat kidney were examined and the results compared with those obtained for the renin in renal extract. 2. In renal extract, two high-molecular-weight reruns (molecular weight 65 000 and 55 000) and one low-molecular-weight renin (molecular weight 39 000) were found. Their relative proportion varied depending on extraction conditions. By acidification, high-molecular-weight renins were converted into low-molecular-weight renin without marked changes in activity. 3. In renal perfusate only low-molecular-weight renin was found after renin stimulation by isoprenaline or anoxia. Inactive renin was not found. 4. Renin in renal extract and perfusate samples were both found to consist of at least four isoenzymes having different isoelectric points (pI). The pI patterns were identical in renal extract and perfusate samples: pI 5.7 (60-70%), 5.5 (15-25%), 5.3 (5-10%) and 5.0-5.2 (2-5%). 5. These results indicate that the native renin secreted by rat kidney consists entirely of the low-molecular-weight and active form comprising multiple isoenzymes with a stable pI pattern.

Effect of Acid, Trypsin and Cold Treatment and of Renin— Plasma Interaction on the Activity of Renin Secreted by Rat Kidney

1979 ◽  
Vol 57 (3) ◽  
pp. 233-240 ◽  
Author(s):  
H. Nakane ◽  
Y. Nakane ◽  
P. Corvol ◽  
J. Menard
Keyword(s):  
Rat Kidney ◽  
Cold Treatment ◽  
Rat Plasma ◽  
Renin Activity ◽  
Trypsin Treatment ◽  
Plasma Interaction ◽  
Isolated Perfused Rat Kidney ◽  
Perfused Rat Kidney ◽  
Inactive Renin ◽  
The Difference

1. Renin release from the isolated perfused rat kidney was markedly stimulated by isoprenaline or anoxia. Renin secreted into the blood-free perfusate was not activated by exposure to cold or dialysis to pH 3·3, suggesting the absence either of cryo- or acid-activatable renin or of factors necessary to activate inactive renin. 2. Trypsin treatment did not change renin concentration in the perfusate samples. 3. When binephrectomized rat plasma was added to perfusate samples before dialysis, renin concentration in the acidified samples was significantly higher than in samples dialysed to pH 6·5. Diminished renin recovery in the latter samples caused this difference. Binephrectomized rat plasma itself had no significant renin activity before or after acid dialysis, indicating the absence of any important extrarenal source of active or acid-activatable renin in rats. 4. Acidification of binephrectomized rat plasma before its addition to the perfusate samples markedly reduced the difference between renin recovery during dialysis to pH 3·3 and dialysis to pH 6·5, indicating that acidification irreversibly inhibited renin inactivation by binephrectomized rat plasma. No net increase in renin concentration was observed in any of our experiments. 5. These results suggest that rat kidney does not secrete inactive renin. They also point to the existence of renin inactivation by rat plasma at neutral pH, which might lead to overestimation of acid-activatable renin in rats.

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.

Release of Active and Inactive Kallikrein from the Isolated Perfused Rat Kidney

1984 ◽  
Vol 66 (2) ◽  
pp. 207-215 ◽  
Author(s):  
B. H. Van Leeuwen ◽  
S. M. Grinblat ◽  
C. I. Johnston
Keyword(s):  
Rat Kidney ◽  
Active Form ◽  
Similar Proportion ◽  
Rat Urine ◽  
Isolated Perfused Rat Kidney ◽  
Inactive Form ◽  
Perfused Rat Kidney ◽  
Kallikrein 2 ◽  
Normal Rat ◽  
Immunological Assays

1. The release of kallikrein into the perfusate and urine of the isolated perfused rat kidney was studied. 2. Comparison between enzymic and immunological assays for kallikrein demonstrated the presence of an enzymically inactive form of kallikrein. 3. Of kallikrein found in normal rat urine 77 ± 4% is active and 23% is in an inactive form. 4. In the isolated perfused rat kidney a similar proportion of active kallikrein (84%) was excreted into the urine but very little enzymically active kallikrein (2%) could be detected in the perfusate. 5. However, significant amounts of enzymically inactive but immunologically reactive kallikrein could be found in the kidney perfusate. The rate of release of kallikrein into the perfusate was approximately one-fifth of the rate of release into the urine. 6. Renin showed a similar pattern of release into the perfusate and urine but the lysosomal enzyme marker acid phosphatase was not detectable. 7. These results show that kallikrein is secreted from the kidney into the circulation as well as being excreted in the urine. However, in urine the enzyme is predominantly in an enzymically active form whereas it is secreted into the circulation in an inactive form.

scholarly journals Effects of cyclosporine and its metabolites in the isolated perfused rat kidney.

1993 ◽  
Vol 4 (2) ◽  
pp. 168-177
Author(s):  
K A Roby ◽  
L M Shaw
Keyword(s):  
Vascular Resistance ◽  
Rat Kidney ◽  
Parent Drug ◽  
Renal Vascular Resistance ◽  
Isolated Perfused Rat Kidney ◽  
Perfused Rat Kidney ◽  
Before And After ◽  
Vascular Obstruction ◽  
Dose Responses ◽  
Renal Vascular

The isolated perfused rat kidney (IPK) was used to study the acute effects of cyclosporin A (CsA) and its metabolites (M1, M17, M18, M21 and M-COOH). GFR, renal vascular resistance, and sodium, potassium and water reabsorption were measured before and after the addition of CsA/metabolites/vehicles. There was no difference in CsA effect (mild decrease in GFR and increase in renal vascular resistance with the inclusion of plasma (10 mL) or whole blood (20 mL) in the albumin perfusate (120 mL). Intralipid was used as the vehicle for CsA and the metabolites because methanol, ethanol, and Cremophor had significant effects on GFR. Intralipid enhanced the effect of CsA 25-fold, giving CsA dose responses comparable to those of human kidneys. This enhanced effect with intralipid was due to vasoconstriction, not vascular obstruction, and was apparently specific to CsA (no enhancement of norepinephrine with Intralipid). The primary metabolites (M1, M17, and M21) caused decreases in GFR comparable to or slightly less than those caused by CsA. The secondary metabolites (M18 and M-COOH) caused more modest declines in GFR. Cyclosporine metabolite levels in patient blood often greatly exceed levels of the parent drug; these studies suggest that the metabolites may contribute significantly to CsA nephrotoxicity in patients.

Electron microscopic study of the membrane glycoproteins in the rat kidney after cisplatin treatment

1989 ◽  
Vol 47 ◽  
pp. 912-913
Author(s):  
S.K. Aggarwal
Keyword(s):  
Alkaline Phosphatase ◽  
Rat Kidney ◽  
Light And Electron Microscopy ◽  
Kidney Tissue ◽  
Membrane Glycoproteins ◽  
Electron Microscopic ◽  
Before And After ◽  
Interstrand Cross Links ◽  
Cross Links

The proposed primary mechanism of action of the anticancer drug cisplatin (Cis-DDP) is through its interaction with DNA, mostly through DNA intrastrand cross-links or DNA interstrand cross-links. DNA repair mechanisms can circumvent this arrest thus permitting replication and transcription to proceed. Various membrane transport enzymes have also been demonstrated to be effected by cisplatin. Glycoprotein alkaline phosphatase was looked at in the proximal tubule cells before and after cisplatin both in vivo and in vitro for its inactivation or its removal from the membrane using light and electron microscopy.Outbred male Swiss Webster (Crl: (WI) BR) rats weighing 150-250g were given ip injections of cisplatin (7mg/kg). Animals were killed on day 3 and day 5. Thick slices (20-50.um) of kidney tissue from treated and untreated animals were fixed in 1% buffered glutaraldehyde and 1% formaldehyde (0.05 M cacodylate buffer, pH 7.3) for 30 min at 4°C. Alkaline phosphatase activity and carbohydrates were demonstrated according to methods described earlier.

Validation of a toxicity testing model by evaluating oxygen supply and energy state in the isolated perfused rat kidney

1991 ◽  
Vol 25 (3) ◽  
pp. 195-204 ◽  
Author(s):  
Takano Takehito ◽  
Nakata Kazuyo ◽  
Kawakami Tsuyoshi ◽  
Miyazaki Yoshifumi ◽  
Murakami Masataka ◽  
...  
Keyword(s):  
Oxygen Supply ◽  
Energy State ◽  
Rat Kidney ◽  
Toxicity Testing ◽  
Testing Model ◽  
Isolated Perfused Rat Kidney ◽  
Perfused Rat Kidney

CHANGES IN THE CONCENTRATION OF PITUITARY AND STEROID HORMONES IN THE FOLLICULAR FLUID OF HUMAN GRAAFIAN FOLLICLES THROUGHOUT THE MENSTRUAL CYCLE

1975 ◽  
Vol 64 (3) ◽  
pp. 555-571 ◽  
Author(s):  
K. P. McNATTY ◽  
W. M. HUNTER ◽  
A. S. McNEILLY ◽  
R. S. SAWERS
Keyword(s):  
Menstrual Cycle ◽  
Steroid Hormones ◽  
Follicular Fluid ◽  
Follicle Stimulating Hormone ◽  
Secretory Activity ◽  
Follicular Phase ◽  
Hormonal Changes ◽  
Peripheral Plasma ◽  
Before And After ◽  
Late Follicular Phase

SUMMARY The concentrations of FSH, LH, prolactin, oestradiol and progesterone were measured in peripheral plasma and follicular fluid of women throughout the menstrual cycle. With the exception of prolactin, concentrations of pituitary and steroid hormones in follicular fluid correlated with those in peripheral plasma. Follicle-stimulating hormone was present in a greater number of small follicles ( < 8 mm) during or just after the peaks of FSH in peripheral plasma. During the mid-follicular phase the concentration of both FSH and oestradiol in fluid from large follicles ( ≥ 8 mm) was high. During the late follicular phase the large follicles ( ≥ 8 mm) contained high amounts of progesterone in addition to oestradiol, low physiological levels of prolactin, and concentrations of LH and FSH about 30 and 60% respectively of those found in plasma. By contrast no large 'active' follicles ( ≥ 8 mm) were found during the luteal phase although many contained both LH and FSH. Luteinizing hormone was present in a proportion of small follicles ( < 8 mm) during the late follicular and early luteal but not at other stages of the menstrual cycle. It is suggested that a precise sequence of hormonal changes occur within the microenvironment of the developing Graafian follicle; the order in which they occur may be of considerable importance for the growth of that follicle and secretory activity of the granulosa cells both before and after ovulation.

SECRETION OF DIHYDROTESTOSTERONE BY HUMAN PROSTATE IN BENIGN PROSTATIC HYPERTROPHY

1974 ◽  
Vol 77 (2) ◽  
pp. 401-407 ◽  
Author(s):  
J. A. Mahoudeau ◽  
A. Delassalle ◽  
H. Bricaire
Keyword(s):  
Plasma Levels ◽  
Benign Prostatic Hypertrophy ◽  
Prostatic Hypertrophy ◽  
Human Prostate ◽  
Control Subjects ◽  
Peripheral Plasma ◽  
Significant Difference ◽  
Before And After ◽  
The Mean ◽  
And Control

ABSTRACT Plasma levels of testosterone (T) and 5α-dihydrotestosterone (DHT) were determined by radioimmunoassay in 29 patients with benign prostatic hypertrophy (BPH) and in 56 control men of various ages. No significant difference was found in T, DHT nor DHT/T ratio between BPH and control subjects of similar age. Plasma DHT was higher in the prostatic than in the peripheral veins in 8/9 patients with BPH during laparotomy, indicating a prostatic secretion of DHT. No difference in the mean T nor the mean DHT was found in peripheral plasma before and after adenomectomy.

Aldosterone Effects on Renal Function in the Isolated Perfused Rat Kidney

1979 ◽  
Vol 2 (1) ◽  
pp. 1-11
Author(s):  
Richard Solomon ◽  
Patricio Silva ◽  
Franklin H. Epstein
Keyword(s):  
Renal Function ◽  
Rat Kidney ◽  
Isolated Perfused Rat Kidney ◽  
Perfused Rat Kidney
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