Longitudinal study of platelet angiotensin II binding in human pregnancy

1992 ◽  
Vol 82 (4) ◽  
pp. 377-381 ◽  
Author(s):  
Philip N. Baker ◽  
Fiona Broughton Pipkin ◽  
E. Malcolm Symonds
Keyword(s):  
Longitudinal Study ◽  
Angiotensin Ii ◽  
Post Partum ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Significant Rise ◽  
Renin Substrate ◽  
Plasma Renin Concentration ◽  
Plasma Angiotensin ◽  
In Pregnancy

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.

Platelet Angiotensin II Binding and Plasma Renin Concentration, Plasma Renin Substrate and Plasma Angiotensin II in Human Pregnancy

1990 ◽  
Vol 79 (4) ◽  
pp. 403-408 ◽  
Author(s):  
Philip N. Baker ◽  
Fiona Broughton Pipkin ◽  
E. Malcolm Symonds
Keyword(s):  
Angiotensin Ii ◽  
Pregnant Women ◽  
Specific Binding ◽  
Plasma Renin ◽  
Second Trimester ◽  
Cross Sectional ◽  
Renin Substrate ◽  
Plasma Renin Concentration ◽  
Plasma Angiotensin ◽  
In Pregnancy

1. The results are presented of a cross-sectional study of 25 non-pregnant and 125 pregnant/postnatal women in whom platelet angiotensin II binding and plasma angiotensin II, plasma renin concentration and plasma renin substrate were measured. 2. Platelet angiotensin II binding was significantly lower in the first-trimester patients as compared with the non-pregnant women (P < 0.001). Specific binding remained low in the second and third trimesters, and in those patients studied 24 h after delivery. However, higher values, approximating to the non-pregnant level, were found 6 weeks postnatally (n = 25 for each group). 3. Plasma angiotensin II, plasma renin concentration and plasma renin substrate increased in pregnancy, with the increase becoming statistically significant as compared with the non-pregnant women in the second trimester. Maximal median values of plasma angiotensin II and plasma renin substrate were found in the third trimester, but maximal median values of plasma renin concentration were found in the second trimester. The concentrations of all three hormones fell after delivery. 4. There was an inverse correlation between platelet angiotensin II binding and simultaneously measured endogenous levels of plasma angiotensin II (P < 0.02) and plasma renin substrate (P < 0.05) in the 25 non-pregnant subjects. These findings support the concept of the angiotensin II receptor concentration being regulated by the plasma angiotensin II level. There was no correlation between platelet angiotensin II binding and plasma renin concentration. 5. In pregnancy, no correlation between platelet angiotensin II binding and plasma angiotensin II, plasma renin concentration or plasma renin substrate was found. This suggests that any regulation by plasma angiotensin II may not operate in pregnancy, when reduced binding concentrations are present. No statistically significant correlation was found at either 24 h or 6 weeks after delivery.

Renin, Angiotensin and Aldosterone in Human Pregnancy and the Menstrual Cycle

1971 ◽  
Vol 16 (3) ◽  
pp. 183-196 ◽  
Author(s):  
J. I. S. Robertson ◽  
R. J. Weir ◽  
G. O. Düsterdieck ◽  
R. Fraser ◽  
M. Tree
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin ◽  
Normal Pregnancy ◽  
Maternal Plasma ◽  
Plasma Aldosterone ◽  
Sodium Depletion ◽  
Aldosterone Secretion ◽  
Renin Substrate ◽  
Plasma Aldosterone Concentration ◽  
In Pregnancy

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.

scholarly journals Local renin-angiotensin system contributes to hyperthyroidism-induced cardiac hypertrophy

1999 ◽  
Vol 160 (1) ◽  
pp. 43-47 ◽  
Author(s):  
H Kobori ◽  
A Ichihara ◽  
Y Miyashita ◽  
M Hayashi ◽  
T Saruta
Keyword(s):  
Angiotensin Ii ◽  
Thyroid Hormone ◽  
Cardiac Hypertrophy ◽  
Plasma Renin Activity ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Plasma Angiotensin ◽  
Renin Mrna

We have reported previously that thyroid hormone activates the circulating and tissue renin-angiotensin systems without involving the sympathetic nervous system, which contributes to cardiac hypertrophy in hyperthyroidism. This study examined whether the circulating or tissue renin-angiotensin system plays the principal role in hyperthyroidism-induced cardiac hypertrophy. The circulating renin-angiotensin system in Sprague-Dawley rats was fixed by chronic angiotensin II infusion (40 ng/min, 28 days) via mini-osmotic pumps. Daily i.p. injection of thyroxine (0.1 mg/kg per day, 28 days) was used to mimic hyperthyroidism. Serum free tri-iodothyronine, plasma renin activity, plasma angiotensin II, cardiac renin and cardiac angiotensin II were measured with RIAs. The cardiac expression of renin mRNA was evaluated by semiquantitative reverse transcriptase-polymerase chain reaction. Plasma renin activity and plasma angiotensin II were kept constant in the angiotensin II and angiotensin II+thyroxine groups (0.12+/-0.03 and 0.15+/-0.03 microgram/h per liter, 126+/-5 and 130+/-5 ng/l respectively) (means+/-s.e.m.). Despite stabilization of the circulating renin-angiotensin system, thyroid hormone induced cardiac hypertrophy (5.0+/-0.5 vs 3.5+/-0.1 mg/g) in conjunction with the increases in cardiac expression of renin mRNA, cardiac renin and cardiac angiotensin II (74+/-2 vs 48+/-2%, 6.5+/-0.8 vs 3.8+/-0.4 ng/h per g, 231+/-30 vs 149+/-2 pg/g respectively). These results indicate that the local renin-angiotensin system plays the primary role in the development of hyperthyroidism-induced cardiac hypertrophy.

Renin–Angiotensin System in Mild Essential Hypertension. the Functional Significance of Angiotensin II in Untreated and Thiazide-Treated Hypertensive Patients

1978 ◽  
Vol 55 (s4) ◽  
pp. 319s-321s ◽  
Author(s):  
H. Ibsen ◽  
A. Leth ◽  
H. Hollnagel ◽  
A. M. Kappelgaard ◽  
M. Damkjaer Nielsen ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Functional Significance ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Plasma Angiotensin

1. Twenty-five patients with mild essential hypertension, identified during a survey of a population born in 1936, were investigated. 2. Basal and post-frusemide values for plasma renin concentration and plasma angiotensin II concentration did not differ markedly from reference values in 25 40-year-old control subjects. In the untreated, sodium replete state saralasin infusion (5·4 nmol min−1 kg−1) produced an increase in mean arterial pressure in the patient group as a whole. 3. Twenty-one patients were treated with hydrochlorothiazide, mean dose 75 mg/day for 3 months. Pre-treatment, frusemide-stimulated plasma renin concentration and plasma angiotensin II, and values during thiazide treatment were higher in ‘non-responders’ (n = 10) to hydrochlorothiazide treatment than in ‘thiazide-responders’ (n = 11). During thiazide therapy, angiotensin II blockade induced a clear-cut decrease in mean arterial pressure in all ‘thiazide-nonresponders’ whereas only four out of 11 ‘thiazide-responders’ showed a borderline decline in mean arterial pressure. 4. The functional significance of the renin—angiotensin system in mild essential hypertension emerges only after thiazide treatment. Thiazide-induced stimulation of the renin—angiotensin system counter-balanced the hypotensive effect of thiazide in some 40% of the treated patients. Thus the responsiveness of the renin—angiotensin system determined the blood pressure response to thiazide treatment.

RENIN LEVELS IN THE KANGAROO, THE WOMBAT AND OTHER MARSUPIAL SPECIES

1971 ◽  
Vol 51 (1) ◽  
pp. 79-90 ◽  
Author(s):  
PAMELA A. SIMPSON ◽  
J. R. BLAIR-WEST
Keyword(s):  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Angiotensin I ◽  
Renin Substrate ◽  
Angiotensin System ◽  
Plasma Renin Concentration ◽  
Red Kangaroo ◽  
Grey Kangaroo ◽  
Common Wombat ◽  
Marsupial Species

SUMMARY A renin—angiotensin system was shown to be present in several marsupial species in plasma and homogenates of the renal cortex. Species studied were: Eastern Grey kangaroo (Macropus giganteus), Red kangaroo (Megaleia rufa), common wombat (Vombatus hirsutus), pademelon (Thylogale billardierii), Bennett's wallaby (Wallabia rufogrisea frutica), a quokka (Setonix brachyurus) and a tiger cat (Dasyurus maculatus). Renin-substrate was found in the plasma of the Eastern Grey kangaroo, the Red kangaroo and the wombat. Renin was shown to be present in the plasma of all species by incubation alone or with heterologous marsupial renin-substrate. Plasma renin concentration and renal renin content were estimated by an established method using standard sheep renin-substrate. Plasma renin concentration was high, suggesting that marsupial renins have a high affinity for sheep substrate; renal renin estimates were low relative to eutherian species, suggesting that renal storage may be small. Plasma renin concentration and renal renin levels were proportionately related. Renin levels were consistently lowest in the wombat. Bilateral nephrectomy of an Eastern Grey kangaroo reduced plasma renin concentration to zero and increased renin-substrate concentration eightfold. The angiotensin-like incubation product from Eastern Grey kangaroo renin-substrate did not cross react with antibodies to [5-Ile]-angiotensin I, suggesting that the product has a different sequence of amino acids.

Effect of methylprednisolone upon arterial pressure and the renin angiotensin system in the rat

1975 ◽  
Vol 228 (2) ◽  
pp. 613-617 ◽  
Author(s):  
LR Krakoff ◽  
R Selvadurai ◽  
E Sutter
Keyword(s):  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Renin Substrate ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Significant Fall ◽  
Arterial Blood ◽  
Methylprednisolone Treatment

The effect of methylprednisolone or deoxycorticosterone upon systemic arterial blood pressure and components of the renin-angiotensin system was studied in the rat. Rats maintained on regular diets given methylprednisolone suspension 20 mg/kg body wt demonstrated a significant increase in arterial pressure of + 37 plus or minus 5 mmHg, mean plus or minus SE, over a 2-wk period, whereas those treated with DOC and untreated controls showed no significant change. On normal diets, plasma renin concentration (PRC) of methylprednisolone-treated rats was significantly higher than that of DOC-treated rats. Methylprednisolone treatment also resulted in a significant elevation of plasma renin substrate concentration (PRS). Calculated plasma renin activity (PRA) was highest in methylprednisolone-treated rats, significantly above that of the DOC and no-steroid groups. NaCl supplementation resulted in a significant fall in PRC and PRA in all three groups; however, PRS remained significantly above normal in the methylprednisolone-treated rats. The pressor effect of angiotensin II was slightly increased in methylprednisolone-treated rats. Infusion of [Sar1,Ala8]angiotensin II (P-113) in methylprednisolone-treated rats resulted in a significant fall in diastolic arterial pressure. The results imply that methylprednisolone hypertension in the rat may be in part angiotensin dependent.

Angiotensin II (AII) and adrenal gland AII receptors in rats with congenital hypothyroidism

1993 ◽  
Vol 137 (2) ◽  
pp. 231-238 ◽  
Author(s):  
M. J. Matilla ◽  
M. Montiel ◽  
E. Jiménez
Keyword(s):  
Angiotensin Ii ◽  
Adrenal Gland ◽  
Congenital Hypothyroidism ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Hormone Deficiency ◽  
Electrolyte Balance ◽  
Renin Substrate ◽  
Receptor Isoforms ◽  
Ace Activity

ABSTRACT Plasma angiotensin II (AII) concentration, plasma renin concentration (PRC), lung angiotensin-converting enzyme (ACE) activity and adrenal gland AII receptor isoforms have been evaluated in the postnatal development of the rat, in order to determine the alterations of the renin-angiotensin system (RAS) which occur in congenital hypothyroidism. The developmental AII profiles observed in control and hypothyroid rats were quite similar. Thus, AII was elevated at birth and declined at week 5 of life to reach adult values. However, AII levels were lower in hypothyroid than in euthyroid animals before their stabilization. On the other hand, PRC in newborn hypothyroid and euthyroid animals was higher than in adulthood, being significantly increased immediately after birth in hypothyroid rats. Pulmonary ACE activity in both experimental groups was low at birth and increased with age. This increase was greater in euthyroid rats than in congenitally hypothyroid animals from day 28 of life. These results confirm that plasma AII levels in rats are predominantly controlled by plasma renin activity, although other factors, such as renin substrate availability, may be responsible for the reduced plasma AII concentration in congenital hypothyroidism during the first weeks of life. The developmental profile of the adrenal gland AII receptor showed four isoforms, with pI values of 6·8, 6·7, 6·5 and 6·3. AII receptor-complex expression increased with age but, in congenitally hypothyroid rats, a higher induction of AII receptor isoforms migrating to pI 6·8, 6·5 and 6·3 was observed. These findings show that thyroid hormone deficiency in early life can have an important role in the postnatal induction of the RAS components, which may be essential for the regulation of blood pressure, and for fluid and electrolyte balance in developing rats. Journal of Endocrinology (1993) 137, 231–238

The Effect of Prostaglandin E2 Upon the Biochemical Response to Infused Angiotensin II in Human Pregnancy

1984 ◽  
Vol 66 (4) ◽  
pp. 399-406 ◽  
Author(s):  
F. Broughton Pipkin ◽  
J. C. Hunter ◽  
S. R. Turner ◽  
P. M. S. O'Brien
Keyword(s):  
Angiotensin Ii ◽  
Prostaglandin E2 ◽  
Plasma Concentrations ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Pressor Effect ◽  
Renin Substrate ◽  
Plasma Aldosterone Concentration ◽  
Plasma Renin Concentration ◽  
Pressure Plasma

1. The effects of angiotensin II infusion without and with simultaneous infusion of prostaglandin E2 were studied in 25 women in second trimester pregnancy. Twenty received one infusion of angiotensin II alone, followed by its infusion simultaneously with prostaglandin E2; five received two identical infusions of angiotensin II alone as controls. 2. Angiotensin II infusion alone was associated with suppression of plasma renin concentration to levels inversely proportional to the evoked change in diastolic blood pressure. Plasma renin substrate concentration was unchanged, but plasma aldosterone concentration rose markedly. This rise was inversely proportional to the threshold for pressor effect of angiotensin II. 3. Prostaglandin E2 administration alone was associated with increased plasma renin concentrations. 4. The pressor effect of angiotensin II was blunted when given together with prostaglandin E2 and plasma concentrations of angiotensin II reached were lower. 5. Plasma renin concentration was again suppressed during the joint infusion regimen; the degree of suppression was inversely proportional to the change in diastolic pressure. Plasma aldosterone concentration rose, but did not differ in the control and experimental groups. 6. Thus although the renin-angiotensin system is stimulated in normal pregnancy, the normal control mechanisms are still functional, and the capacity for further increases in activity exists.

Plasma Renin and Angiotensin Levels in Human Hypertension following Treatment

1973 ◽  
Vol 45 (s1) ◽  
pp. 287s-290s
Author(s):  
C. I. Johnston ◽  
N. Anavekar ◽  
K. G. Chua ◽  
W. J. Louis
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Plasma Catecholamines ◽  
Plasma Renin ◽  
Significant Rise ◽  
Renin Activity ◽  
Adrenergic Blockade ◽  
Renin Substrate ◽  
Close Relationship ◽  
Plasma Angiotensin

1. The levels of plasma renin activity or concentration and plasma angiotensin were similar in normotensive subjects and in untreated or treated essential hypertensives. 2. There was a close relationship between plasma renin activity and plasma renin concentration and between these and plasma angiotensin. This suggests that there were no abnormalities in renin substrate or renin kinetics in human essential hypertension. 3. Ganglion blockade did not change the plasma renin levels but α-adrenergic blockade caused a significant rise in plasma catecholamines and plasma renin without change in blood pressure. 4. Both acute and chronic β-adrenergic blockade were associated with a fall in blood pressure and small but significant falls in plasma renin levels.

The response of the Renin-Angiotensin System in Rats to the Injection of Angiotensin II Antibodies

1974 ◽  
Vol 48 (s2) ◽  
pp. 27s-30s
Author(s):  
E. Hackenthal ◽  
H. Bauknecht ◽  
P. Oster
Keyword(s):  
Angiotensin Ii ◽  
Binding Capacity ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Distribution Volume ◽  
Antibody Concentration ◽  
Half Time ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Plasma Angiotensin

1. Antibodies against angiotensin II were purified by affinity chromatography. 2. When injected intravenously into rats, the antibody distributed in the extracellular space with a half-time of 11 h and a distribution volume of about 10 ml/100 g body weight. The antibody was eliminated with a half-time of 7 days. 3. Plasma angiotensin II concentrations increased about 100-fold the control values 7 min after antibody injection and declined in parallel with the antibody concentration. It was calculated that only about 1–4% of the binding capacity of the antibody was occupied by angiotensin throughout the experiment. 4. Since the plasma renin concentration was normal, except during the short initial phase of stimulation, it is concluded that upon antibody injection the renin-angiotensin system rapidly, reached an equilibrium, with concentrations of free angiotensin close to or identical with normal concentrations.

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