Renal Release of Active and Inactive Renin in Essential and Renovascular Hypertension

1978 ◽  
Vol 55 (s4) ◽  
pp. 129s-132s ◽  
Author(s):  
F. H. M. Derkx ◽  
R. P. Verhoeven ◽  
G. J. Wenting ◽  
A. J. Man in 't Veld ◽  
M. A. D. H. Schalekamp
Keyword(s):  
Essential Hypertension ◽  
Renovascular Hypertension ◽  
Intravenous Injection ◽  
Renal Vein ◽  
Active Renin ◽  
A Value ◽  
Affected Side ◽  
Inactive Renin ◽  
Arterial Plasma

1. Active and acid-activable inactive renin were measured in renal venous and arterial plasma of 18 patients with essential hypertension (EHT) and 19 patients with renovascular hypertension (RVHT). In seven patients with EHT and in 11 patients with RVHT measurements were made before and 25–35 min after an intravenous injection of 300 mg of diazoxide. 2. Under basal conditions the renal vein to artery ratios for active and inactive renin in EHT ranged from 0·71 to 1·96 and from 0·68 to 1·44 respectively. In 14 patients with RVHT the renal vein to artery ratio for active renin on the affected side was above the range found in EHT and in six of them the renal vein to artery ratio for inactive renin was also elevated. 3. The diazoxide-induced release of active renin from kidneys, which had a stenotic artery but were not seriously contracted, was associated with a fall of the renal vein to artery ratio for inactive renin to a value below 1·00. 4. The results indicate that changes in the release of active and inactive renin do not always run in parallel. The findings are compatible with the hypothesis that circulating inactive renin can be activated in the kidney.

Control of Enzymatically Inactive Renin in man under Various Pathological Conditions: Implications for the Interpretation of Renin Measurements in Peripheral and Renal Venous Plasma

1978 ◽  
Vol 54 (5) ◽  
pp. 529-538 ◽  
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):  
Essential Hypertension ◽  
Renovascular Hypertension ◽  
Renal Vein ◽  
Plasma Renin ◽  
Peripheral Vein ◽  
Native Form ◽  
Mean Values ◽  
Active Renin ◽  
Affected Side ◽  
Inactive Renin

1. Human plasma contains two types of renin: one is active in its native form (active renin), the other has renin-like activity after exposure to low pH (inactive renin). Reactions of acid-activated plasma renin and kidney renin with either homologous or heterologous substrate showed identical Km values. 2. Peripheral venous values for active and inactive renin in essential hypertension (n = 22), renovascular hypertension (n = 14), primary aldosteronism (n = 12), adrenal insufficiency (n = 6) and control subjects (n = 13) were directly correlated. But the percentage of renin that was active varied widely. 3. After bilateral nephrectomy in 12 patients both active and inactive plasma renin fell, but did not completely disappear. Estimates of half-life in two patients were 30–80 min for active renin and 150–165 min for inactive renin. 4. Renal vein to peripheral vein ratios of active and inactive renin in ten patients with essential hypertension (19 determinations) ranged from 0·96 to 1·60 and from 0·68 to 1·44 respectively with mean values (±sem) of 1·21 ± 0·04 and 1·06 ± 0·05. 5. The renal vein to peripheral vein ratio of active renin on the affected side in 13 out of 17 patients with renovascular hypertension was above the range found in essential hypertension. Six of them also had an elevated ratio of inactive renin on that side, which indicated renal release of this form of renin into the circulation. But, in contrast to the renal vein to peripheral vein ratio of active renin, the mean value of the ratio of inactive renin on the affected side was not significantly higher than on the contralateral side. The results suggest a renal mechanism not only for controlling the total quantity of circulating renin but also for modulating its degree of activation.

Uptake of Inactive Renin by Human Ischaemic Kidney

1983 ◽  
Vol 65 (1) ◽  
pp. 27-32 ◽  
Author(s):  
I. M. McKenzie ◽  
E. Reisin ◽  
J. K. McKenzie
Keyword(s):  
Essential Hypertension ◽  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Peripheral Blood ◽  
Renal Vein ◽  
Vena Cava ◽  
Artery Stenosis ◽  
Renal Ischaemia ◽  
Active Renin ◽  
Inactive Renin

1. Plasma samples from both renal veins and infrarenal inferior vena cava were studied in 21 patients with unilateral renal artery stenosis and 11 patients without significant renal artery stenosis (essential hypertension), both groups being on unrestricted sodium intake. 2. Whether inactive renin was activated by acid or trypsin, it tended to be increased by 50–100% in unilateral renal ischaemia patients compared with essential hypertension. Active renin was increased two- to four-fold in unilateral renal ischaemia patients compared with those with essential hypertension. Thus the ratio of active to total renin in peripheral venous blood tended to be higher in unilateral renal ischaemia (0.37) than in essential hypertension (0.30) patients. 3. in renal vein blood from the affected kidney in unilateral renal ischaemia, the proportion of active renin to total renin was very high (68% for trypsinized samples and 73% for acidified samples). When affected renal vein blood was compared with infrarenal vena caval blood (equivalent to renal artery blood in amount and proportions of active and inactive renin), there was found to be a marked increase of active renin (ratio 2.83, significance of difference from 1.0, P < 0.001), as expected. 4. Inactive renin was decreased in affected renal vein blood compared with peripheral blood (ratio of renal vein to peripheral blood renin). This occurred whether acidification was used (ratio 0.62 ±0.11, P < 0.01) or trypsin (ratio 0.70 ± 0.13, P < 0.05). 5. The cause of the apparent uptake may be conversion of inactive renin into active renin by protease action in the ischaemic kidney. Urinary excretion or lymphatic drainage would seem unlikely.

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.

scholarly journals Renal vein plasma renin activity in patients with essential hypertension and renovascular hypertension.

1986 ◽  
Vol 75 (6) ◽  
pp. 728-732
Author(s):  
Ko SATO ◽  
Keishi ABE ◽  
Masahide SEINO ◽  
Minoru YASUJIMA ◽  
Yutaka IMAI ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Plasma Renin Activity ◽  
Renovascular Hypertension ◽  
Renal Vein ◽  
Plasma Renin ◽  
Renin Activity

Release of Active and Inactive Renin by the Human Kidney

1979 ◽  
Vol 57 (s5) ◽  
pp. 101s-103s ◽  
Author(s):  
W. Aoi ◽  
S. Seto ◽  
Y. Doi ◽  
M. Murayama ◽  
S. Tasaki ◽  
...  
Keyword(s):  
Inferior Vena Cava ◽  
Inferior Vena ◽  
Vena Cava ◽  
Human Kidney ◽  
Upright Position ◽  
Renal Veins ◽  
Active Renin ◽  
Affected Side ◽  
Inactive Renin ◽  
Renal Abnormalities

1. Active and inactive renin were assayed in plasma of the renal veins and the inferior vena cava below the kidney in eight patients with hypertension and unilateral renal abnormalities, 20 min after the patients had resumed the upright position. 2. The concentration of active renin on the affected side was significantly higher than that on the non-affected side. The concentration of inactive renin on the affected side was significantly lower than that on the non-affected side and in the inferior vena cava. 3. These findings suggest either that the affected kidney mainly secretes active renin, which is then converted into inactive renin in the extrarenal circulation, or that the affected kidney activates 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.

RENAL-VEIN RENIN IN RENOVASCULAR HYPERTENSION

The Lancet ◽  
1966 ◽  
Vol 287 (7452) ◽  
pp. 1429 ◽  
Author(s):  
Philippe Meyer ◽  
Paul Milliez ◽  
JeanM. Alexandre ◽  
Claudine Devaux
Keyword(s):  
Renovascular Hypertension ◽  
Renal Vein ◽  
Renal Vein Renin

RENOVASCULAR HYPERTENSION IN CHILDREN

PEDIATRICS ◽  
1970 ◽  
Vol 46 (3) ◽  
pp. 362-370
Author(s):  
Ernst P. Leumann ◽  
Robert P. Bauer ◽  
Paul E. Slaton ◽  
Edward G. Biglieri ◽  
Malcolm A. Holliday
Keyword(s):  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Renovascular Hypertension ◽  
Pediatric Patient ◽  
Renal Vein ◽  
Diagnostic Problem ◽  
Bilateral Renal Artery Stenosis ◽  
Bilateral Renal Artery ◽  
Fibromuscular Hyperplasia ◽  
Hypertension In Children

Three children with renovascular hypertension are presented in order to demonstrate the wide clinical spectrum of this disease. Two patients had relatively minor symptoms, but one with neurofibromatosis showed frank hypokalemia, polyuria, and hyponatremia. Three different anatomical lesions were found: bilateral renal artery stenosis in the patient with neurofibromatosis, fibromuscular hyperplasia in the patient with stenosis of one renal artery, and an isolated malformation of one small intrarenal artery. The last of our patients presented a complicated diagnostic problem which required repeated arteriograms and renal vein catheterizations for differential renin assay. Renovascular hypertension should be excluded in any pediatric patient with otherwise unexplained hypertension.

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