Renin, Renin Substrate and Angiotensin II Concentration in Renal Venous Blood

Author(s):  
W. Oelkers ◽  
C. Holze ◽  
M. Molzahn ◽  
R. Soerensen
1969 ◽  
Vol 61 (1_Suppl) ◽  
pp. S120
Author(s):  
M. D. Cain ◽  
K. J. Catt ◽  
J. P. Coghlan

1988 ◽  
Vol 255 (4) ◽  
pp. F749-F754 ◽  
Author(s):  
H. M. Siragy ◽  
N. E. Lamb ◽  
C. E. Rose ◽  
M. J. Peach ◽  
R. M. Carey

ACRIP is a competitive inhibitor of renin in which an analogue of statine, (3R,4S)-4-amino-3-hydroxy-6-methylheptanoic acid, is incorporated into analogues of porcine renin substrate. ACRIP inhibits the enzymatic activity of renin, thus blocking the initiation of the angiotensin cascade. We studied the intrarenal action of ACRIP in small quantities without measurable systemic effects on renal function. In the first experiment, ACRIP was administered intrarenally at 0.02, 0.2, and 2 micrograms.kg-1.min-1 to uninephrectomized conscious dogs (n = 6) in metabolic balance at sodium intake of 10 meq/day. ACRIP, in doses of 0.02 and 0.2 micrograms.kg-1.min-1, markedly increased urine sodium excretion (UNaV) from 5.8 +/- 1.4 to 15.1 +/- 5.1 and 19.9 +/- 3.2 mu eq/min, respectively. Urinary flow rate (UV) underwent a similar increase and glomerular filtration rate (GFR) increased from 25.7 +/- 2.5 to 35.6 +/- 2.5 at 0.02 micrograms.kg-1.min-1 of ACRIP. Renal plasma flow (RPF), plasma renin activity (PRA), and plasma aldosterone concentration (PAC) were not affected. At 2 micrograms.kg-1.min-1, ACRIP traversed the kidney in quantities large enough to produce a reduction in systemic PRA and mean arterial pressure and caused natriuresis, diuresis, and increased GFR. In a second experiment, ACRIP was administered intrarenally at 0.2 micrograms.kg-1.min-1 in a separate group (n = 4) under identical conditions. ACRIP-induced increases in UV and UNaV were completely blocked by concurrent intrarenal administration of angiotensin II. The results indicate that intrarenal angiotensin II acts as a physiological regulator of renal sodium and fluid homeostasis.


1971 ◽  
Vol 16 (3) ◽  
pp. 183-196 ◽  
Author(s):  
J. I. S. Robertson ◽  
R. J. Weir ◽  
G. O. Düsterdieck ◽  
R. Fraser ◽  
M. Tree

Aldosterone secretion is frequently, although not invariably, increased above the normal non-pregnant range in normal pregnancy. Substantial increases in plasma aldosterone concentration have also been demonstrated as early as the sixteenth week. In pregnancy, aldosterone secretion rate responds in the usual way to changes in sodium intake. Plasma renin concentration is frequently, but not invariably, raised above the normal non-pregnant range. Plasma renin-substrate is consistently raised in pregnancy. Plasma angiotensin II has also been shown usually to be raised in a series of pregnant women. A significant positive correlation has been shown between the maternal plasma aldosterone concentration and the product of the concurrent plasma renin and renin-substrate concentrations. This suggests that the increased plasma aldosterone in pregnancy is the consequence of an increase in circulating angiotensin II, which in turn is related to the level of both renin and its substrate in maternal blood. For these reasons, estimations of renin activity in pregnancy are of dubious value. The increased renin, angiotensin and aldosterone concentrations may represent a tendency to maternal sodium depletion, probably mainly a consequence of the increased glomerular filtration rate. It is possible that the nausea and other symptoms of early pregnancy may be a consequence of this tendency to sodium depletion, with its attendant hormonal changes. In ‘pre-eclampsia’, renin and aldosterone values are generally slightly lower than in normal pregnancy. Human chorion can apparently synthesize renin independently of the kidney. The physiological significance of this remains at present obscure, but it seems unlikely that this source contributes much, if at all, to the often elevated maternal plasma renin. Plasma renin, renin-activity and angiotensin II concentrations, and aldosterone secretion are increased in the luteal phase of the menstrual cycle.


1992 ◽  
Vol 82 (4) ◽  
pp. 377-381 ◽  
Author(s):  
Philip N. Baker ◽  
Fiona Broughton Pipkin ◽  
E. Malcolm Symonds

1. Platelet angiotensin II binding, circulating angiotensin II levels, plasma renin substrate and plasma renin concentration were measured in a longitudinal study of 30 women during pregnancy and the puerperium. 2. There was a significant fall in platelet angiotensin II binding from 11 weeks gestation to 18 weeks gestation (P < 0.01). There were no further significant changes in platelet angiotensin II binding until after delivery, a significant rise in platelet angiotensin II binding being found at 6 weeks post partum as compared with at 36 weeks gestation (P < 0.01). There was no further significant change from 6 to 12 weeks post partum, and platelet angiotensin II binding at 6 and 12 weeks post partum in the pregnant cohort approximated to that in non-pregnant women. These changes parallel those known to occur in pressor responsiveness to angiotensin II in pregnancy. 3. Plasma angiotensin II concentration, plasma renin substrate and plasma renin concentration were all significantly higher during pregnancy than in the puerperium (P < 0.001). There were no significant changes during pregnancy in plasma angiotensin II concentration or plasma renin concentration, although plasma renin substrate rose throughout. 4. Significant inverse correlations between platelet angiotensin II binding and plasma angiotensin II concentration (P < 0.01), plasma renin substrate (P < 0.01) and plasma renin concentration (P 0>001) were found during pregnancy. These data suggest that down-regulation of platelet angiotensin II binding by the components of the renin-angiotensin system pertains in pregnancy. 5. We are currently investigating parallelism between platelet and vascular angiotensin-binding sites. If such is confirmed, studies of platelet angiotensin II binding in pregnancy may be of both basic physiological and clinical interest in relation to the hypertensive diseases of pregnancy.


1968 ◽  
Vol 40 (1) ◽  
pp. 1-13 ◽  
Author(s):  
D. PAULINE ALEXANDER ◽  
H. G. BRITTON ◽  
V. H. T. JAMES ◽  
D. A. NIXON ◽  
R. A. PARKER ◽  
...  

SUMMARY From the left adrenal of ten sheep foetuses and four lambs aged from 110 days after conception to 14 days after birth, adrenal venous blood was collected and assayed for cortisol, corticosterone and aldosterone. These steroids were secreted at all ages but the rate of secretion was greatly increased toward term and after birth. The increase coincided with morphological changes in the adrenal gland. At no stage was the rate significantly increased by corticotrophin, and in two young foetuses it was not decreased by dexamethasone. In two foetuses and one lamb, angiotensin II did not increase the rate of secretion of any of the three steroids significantly, and the blood pressure was raised only in the lamb. It is probable that the secretion of the steroids was maximal under the conditions of the experiments.


1981 ◽  
Vol 61 (s7) ◽  
pp. 273s-275s ◽  
Author(s):  
W. Oelkers ◽  
A. Köhler ◽  
L. Belkien ◽  
R. Fuchs-Hammoser ◽  
M. Maiga ◽  
...  

1. Adrenocorticotropic hormone (ACTH; 10 i.u./day) was infused for 34 h into normal male subjects. Some subjects were additionally treated with propranolol or indomethacin. Others received sham infusions or hydrocortisone infusions instead of ACTH. 2. ACTH, but not sham or hydrocortisone infusions, led to a significant increase in plasma renin activity and angiotensin II concentration with a lag period of 7–10 h and a maximum response after 24 h. ACTH may be a physiological regulator of renin secretion, perhaps through a ‘trophic’ effect on the juxtaglomerular apparatus. 3. The effect of ACTH on renin is not mediated by a rise in plasma renin substrate, probably not by renal β-adrenoreceptors, but perhaps by prostaglandins. 4. A dissociation between plasma cortisol and aldosterone during ACTH infusion suggests that ACTH, in this dosage, stimulates aldosterone on the second day through renin and angiotensin II, before its secretion is finally suppressed during more prolonged infusion.


1973 ◽  
Vol 45 (1) ◽  
pp. 51-64 ◽  
Author(s):  
M. A. Waite

1. A radioimmunoassay for angiotensin I is described. 2. An extraction procedure for angiotensin I from blood was developed, using alcoholic precipitation to stop the renin/renin substrate reaction. 3. The normal range found for angiotensin I in venous blood was 11–88 pg/ml and in arterial blood 12–72 pg/ml. 4. Angiotensin I levels fell following bilateral nephrectomy but angiotensin I was still detected several weeks following operation.


1977 ◽  
Vol 52 (5) ◽  
pp. 449-456 ◽  
Author(s):  
Fiona Broughton Pipkin ◽  
E. M. Symonds

1. A radioimmunoassay for the measurement of angiotensin II in 1 ml of plasma has been developed and used to measure angiotensin II in maternal peripheral, cord venous and cord arterial blood in 45 patients at delivery. 2. In babies delivered vaginally, cord venous and cord arterial concentrations of angiotensin II were significantly higher than maternal venous blood concentrations. There was a significant relationship between both cord venous and cord arterial concentrations and maternal concentrations of angiotensin II. 3. Cord venous concentrations of angiotensin II were significantly greater than those in cord arterial blood in babies delivered vaginally but not in those delivered by lower-segment Caesarean section. This suggests the possibility that, during labour, the placenta may contribute to foetal concentrations of angiotensin II. 4. Maternal and cord venous concentrations of angiotensin II were significantly higher in patients with hypertensive disease of pregnancy than in those who had remained normotensive throughout pregnancy. 5. Cord venous concentrations of angiotensin II increased significantly with increasing duration of the second stage of labour.


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