Evidence for two independent effects of oestradiol benzoate on the renin-angiotensin-aldosterone system

1982 ◽  
Vol 100 (1) ◽  
pp. 77-84 ◽  
Author(s):  
Helmut Kaulhausen ◽  
Cornelia Weyand
Keyword(s):  
Time Course ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Renin Substrate ◽  
Renin Angiotensin Aldosterone System ◽  
Plasma Aldosterone Concentration ◽  
Renin Angiotensin ◽  
Oestradiol Benzoate ◽  
Independent Effects

Abstract. Plasma renin concentrations (PRC), plasma renin substrate concentration (PRS), plasma aldosterone and cortisol concentrations as well as plama renin activity (PRA) were measured in ovariectomized subjects after im administration of 10 mg oestradiol benzoate (EB). The esterified oestrogen exerts two independent effects on the renin-angiotensin-aldosterone system. 1) 48 h after EB administration, PRS was significantly increased. Similar results were obtained for total plasma cortisol, reflecting transcortin concentration. In both cases, the increase was quantitatively related to the basal concentrations. These observations are consistent with the well known oestrogen-induced protein synthesis in the liver. 2) The elevation of PRC preceded that of PRS and was already significant 11 h after EB injection. The early rise in plasma renin activity was essentially caused by the increase in PRC, whereas an influence of the activated substrate synthesis was found later, between the 2nd and the 4th day post injection. The time course of plasma aldosterone concentration correlated well with the increased PRA. The results provide evidence that EB has two different effects on the renin-aldosterone axis: an early one by elevating renin release and a delayed one by increasing renin substrate synthesis. Whereas the second mechanism can clearly be localized in the liver, extrarenal as well as direct renal effects of EB may be responsible for the renin stimulation.

Inhibition of the Renin-Angiotensin-Aldosterone System by l-Dopa with and without Inhibition of Extracerebral Dopa Decarboxylase in Man

1981 ◽  
Vol 61 (2) ◽  
pp. 187-190 ◽  
Author(s):  
C. Barbieri ◽  
R. Caldara ◽  
C. Ferrari ◽  
Rosa Maria Crossignani ◽  
M. Recchia
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Plasma Aldosterone ◽  
Renin Angiotensin Aldosterone System ◽  
Plasma Aldosterone Concentration ◽  
Renin Angiotensin ◽  
Drugs Analysis ◽  
Catecholamine Levels

1. The present study was undertaken to investigate the possibility that central nervous system mono-aminergic pathways may play a role in the control of the renin-angiotensin-aldosterone system in man. 2. Eight normal subjects received in a randomized order placebo, l-dopa (500 mg, orally) and l-dopa (100 mg, orally) plus carbidopa (35 mg, orally) after pretreatment with carbidopa (50 mg every 6 h for four doses). 3. l-Dopa administration elicited a significant fall in plasma renin activity (PRA) (P < 0.01 at 120, 150 and 180 min) and in plasma aldosterone levels (P < 0.05 at 90, 120, 150 and 180 min); L-dopa plus carbidopa induced a decrease in PRA (P < 0.05 at 120 and 150 min, P < 0.01 at 180 min) and in plasma aldosterone concentration (P < 0.05 at 30 and 60 min, P < 0.01 at 90 and 120 min), in comparison with placebo administration; between-drugs analysis revealed no difference in the decreases in PRA and plasma aldosterone levels induced by the two regimens. 4. Since l-dopa, as well as l-dopa plus carbidopa, has been shown to augment catecholamine levels in the brain of various animal species, the present data suggest that in man PRA and plasma aldosterone concentration might be inhibited by increased central nervous system catecholamine levels.

scholarly journals RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM IN PATIENTS WITH ABDOMINAL OBESITY AND ARTERIAL HYPERTENSION

2013 ◽  
Vol 19 (5) ◽  
pp. 389-396 ◽  
Author(s):  
E. A. Bazhenova ◽  
O. D. Belyaeva ◽  
A. V. Berezina ◽  
T. L. Karonova ◽  
D. A. Kolodina ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Obese Patients ◽  
Renin Angiotensin Aldosterone System ◽  
Plasma Aldosterone Concentration ◽  
Renin Angiotensin ◽  
Primary Disorder ◽  
Per Se ◽  
Design And Methods

Objective. The activity of renin-angiotensin-aldosterone system (RAAS) is increased in patients with ab-dominal obesity (AO). However, till present time it is unclear whether RAAS activation or hypertension (HTN) found in 50 % patients is the primary disorder.Design and methods. We have studied plasma renin activity (PRA), plasma aldosterone concentration (PAC), their ratio PAC/PRA in patients with AO and related HTN and in subjects without AO.Results. PRA was higher in patients with AO versus people without obesity (2,5 ± 0,2 and 1,7 ± 0,7 ng/ml/hr, p = 0,013), there was a tendency to the reduction of the ratio PAC/PRA in obese patients (14,6 ± 0,9 and 19,7 ± 3,3, p = 0,08). In the subgroup of patients with AO and HTN the PRA was higher, and the ratio PAC/PRA was lower than in obese patients without HTN (PRA: 3,3 ± 0,4 and 1,7±0,2 ng/ml/hr, p = 0,005; PAC/PRA: 11,4 ± 1,1 and 17,4 ± 1,4, p < 0,0001). PRA and systolic blood pressure positively correlated. In patients with morbid obesity (3 degree according to the WHO classiication) obesity may play a signiicant role in the increase of RAAS activity, especially in the absence of concomitant HTN. The ratio PAC/PRA in over weight patients with AO was higher than in patients with AO and body mass index ? 30,0 kg/m (17,2 ± 1,7 and 12,5 ± 1,0 kg/m, p = 0,04). PRA was higher only in patients with AO and co-existing hypertension (3,4 ± 0,7 and 1,1 ± 0,2 ng/ml/hr, p = 0,04).Conclusions. RAAS activity is increased in patients with AO, also due to the co-existing HTN. However, in the absence of elevated blood pressure obesity per se may play a signiicant role in RAAS hyperactivity.

Renin, aldosterone, electrolyte, and cortisol responses to hypoxic decompression

1977 ◽  
Vol 43 (3) ◽  
pp. 421-424 ◽  
Author(s):  
J. R. Sutton ◽  
G. W. Viol ◽  
G. W. Gray ◽  
M. McFadden ◽  
P. M. Keane
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Cortisol ◽  
Acute Mountain Sickness ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Plasma Sodium ◽  
Plasma Aldosterone Concentration ◽  
Urinary Potassium ◽  
Mountain Sickness

Responses of plasma renin activity, plasma aldosterone, plasma cortisol, and plasma electrolyte concentration and urinary electrolyte and aldosterone excretion were studied in four men during hypoxic decompression to a stimulated altitude of 4,760 m in a pressure chamber. Three of the four subjects developed significant acute mountain sickness. Plasma sodium and potassium concentrations were unchanged. No significant change in plasma renin activity was observed, but values tended to fall. Plasma aldosterone concentration was depressed while plasma cortisol was elevated and diurnal variation lost. Urinary sodium excretion was unchanged, but urinary potassium and aldosterone excretion were decreased. The decrease in plasma and urinary aldosterone and urinary potassium in the absence of change in plasma renin activity or plasma potassium is of uncertain origin. It is unlikely to be due to a decrease in adrenocorticotropin secretion since plasma cortisol rose during the same time. None of the changes could be causally implicated in the development of acute mountain sickness although the increase in plasma cortisol was greatest in the most ill.

Factors affecting Potassium Balance During Frusemide Administration

1984 ◽  
Vol 67 (2) ◽  
pp. 195-203 ◽  
Author(s):  
Christopher S. Wilcox ◽  
William E. Mitch ◽  
Ralph A. Kelly ◽  
Paul A. Friedman ◽  
Paul F. Souney ◽  
...  
Keyword(s):  
Salt Intake ◽  
Normal Subjects ◽  
Plasma Aldosterone ◽  
High Salt ◽  
Renin Angiotensin Aldosterone System ◽  
Plasma Aldosterone Concentration ◽  
Water Load ◽  
Renin Angiotensin ◽  
High Salt Intake ◽  
Low Salt

1. We investigated the effects of Na+ intake, the renin-angiotensin-aldosterone system and antidiuretic hormone (ADH) on K+ balance during 3 days of frusemide administration to six normal subjects. Subjects received 40 mg of frusemide for 3 days during three different protocols: Na+ intake 270 mmol/day (high salt); Na+ intake 20 mmol/day to stimulate the renin-angiotensin-aldosterone system (low salt); Na+ intake 270 mmol/day plus captopril (25 mg/6 h) to prevent activation of the renin-angiotensin-aldosterone system. In a fourth protocol, a water load was given during high salt intake to prevent ADH release and then frusemide was given. 2. During high salt intake, frusemide increased K+ excretion (UKV) over 3 h, but the loss was counterbalanced by subsequent renal K+ retention so that daily K+ balance was neutral. 3. During low salt intake, the magnitude of the acute kaliuresis following the first dose of frusemide and the slope of the linear relationship between UKV and the log of frusemide excretion were increased compared with that found during the high salt intake. In addition, low salt intake abolished the compensatory renal retention of K+ after frusemide and cumulative K+ balance over 3 days of diuretic administration was uniformly negative (−86 ± 7 mmol/3 days; P < 0.001). 4. Captopril abolished the rise in plasma aldosterone concentration induced by frusemide. The acute kaliuresis after frusemide was unchanged compared with that observed during high salt intake. The compensatory reduction in UKV occurring after the diuretic was slightly potentiated. In fact, captopril given without the diuretic induced a small positive K+ balance. 5. When a water load was given concurrently with frusemide, the acute kaliuresis was >30% lower compared with that seen with frusemide alone, even though the natriuretic response was unchanged. 6. We conclude that: (a) K+ balance is maintained when frusemide is given during liberal Na+ intake because acute K+ losses are offset by subsequent renal K+ retention; (b) this compensatory K+ retention can be inhibited by aldosterone release which could account for the negative K+ balance seen during salt restriction; (c) the short-term kaliuretic response to frusemide is augmented by release of both ADH and aldosterone whereas changes in K+ balance over 3 days of frusemide are dependent on plasma aldosterone concentration.

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 Hypertension Accompanied by Hyperaldosteronism, Hyperkalemia, and Hyperchloremic Acidosis: A Case Report and Literature Review

2020 ◽  
Vol 2020 ◽  
pp. 1-6
Author(s):  
Yunyun Yang ◽  
Yang Ou ◽  
Yan Ren ◽  
Haoming Tian ◽  
Tao Chen
Keyword(s):  
Metabolic Acidosis ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Heterozygous Mutation ◽  
Plasma Aldosterone Concentration ◽  
First Case ◽  
Whole Exome ◽  
Exon 11 ◽  
Clinical Problems

This study reported on a 24-year-old woman who complained of a paroxysmal headache for six months and elevated blood pressure for four months. Laboratory examination revealed increased serum potassium and chloride levels, metabolic acidosis, suppressed renin activity, and increased plasma aldosterone concentration. Whole-exome sequencing revealed a heterozygous mutation in exon 11 of the KLHL3 gene: c.1298G > A. After treatment with low-dose hydrochlorothiazide, her clinical problems were controlled. This patient is the first case of Gordon syndrome (GS) within the Chinese population caused by a heterozygous KLHL3 mutation. A systematic review of the published literature identified 27 patients with GS caused by a KLHL3 mutation. These patients had a mean age of 28.2 ± 22.0 years; 74.1% presented with hypertension, 76.9% with hyperkalemia, and 59.1% with metabolic acidosis. The patients also had varying levels of plasma renin activity and plasma aldosterone concentrations.

Independence of salt intake induced by calcium deprivation from the renin-angiotensin-aldosterone system

1993 ◽  
Vol 264 (3) ◽  
pp. R492-R499 ◽  
Author(s):  
M. G. Tordoff ◽  
D. M. Pilchak ◽  
R. L. Hughes
Keyword(s):  
Salt Intake ◽  
Plasma Renin ◽  
Calcium Deficiency ◽  
Plasma Aldosterone ◽  
Sodium Balance ◽  
Plasma Sodium ◽  
Receptor Blockade ◽  
Renin Angiotensin Aldosterone System ◽  
Angiotensin System ◽  
Renin Angiotensin

We investigated whether the elevated NaCl intake shown by calcium-deprived rats is mediated by the renin-angiotensin-aldosterone system. First, we looked for manifestations of altered renin-angiotensin-aldosterone system activity during the progression of calcium deficiency. There were no differences between control and calcium-deprived rats in plasma aldosterone concentrations, plasma renin activity, plasma sodium concentrations, sodium balance, or blood pressure. Second, we used selective pharmacological antagonists to examine whether disruption of the renin-aldosterone-angiotensin system influenced salt intake. Blockade of aldosterone receptors with spironolactone (25 mg.kg-1 x day-1 sc for 7 days) had no effect on NaCl intake of control or calcium-deprived rats. Angiotensin AT1 receptor blockade with losartan potassium (0.5-10 mg/kg orally) had no effect on NaCl intake of control or calcium-deprived rats but doses > 0.5 mg/kg decreased NaCl intake of adrenalectomized rats. Taken together, these findings indicate that the renin-angiotensin-aldosterone system does not mediate the increased NaCl intake produced by calcium deficiency. The appetite for salt produced by calcium deficiency involves a different physiological substrate from most other models of NaCl intake.

scholarly journals Effects of Ramipril on the Aldosterone/Renin Ratio and the Aldosterone/Angiotensin II Ratio in Patients With Primary Aldosteronism

Hypertension ◽  
2020 ◽  
Vol 76 (2) ◽  
pp. 488-496 ◽  
Author(s):  
Zeng Guo ◽  
Marko Poglitsch ◽  
Diane Cowley ◽  
Oliver Domenig ◽  
Brett C. McWhinney ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Ace Inhibitors ◽  
Primary Aldosteronism ◽  
Characteristic Curve ◽  
False Negative ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Plasma Aldosterone Concentration

The aldosterone/renin ratio (ARR) is currently considered the most reliable approach for case detection of primary aldosteronism (PA). ACE (Angiotensin-converting enzyme) inhibitors are known to raise renin and lower aldosterone levels, thereby causing false-negative ARR results. Because ACE inhibitors lower angiotensin II levels, we hypothesized that the aldosterone/equilibrium angiotensin II (eqAngII) ratio (AA2R) would remain elevated in PA. Receiver operating characteristic curve analysis involving 60 patients with PA and 40 patients without PA revealed that the AA2R was not inferior to the ARR in screening for PA. When using liquid chromatography-tandem mass spectrometry to measure plasma aldosterone concentration, the predicted optimal AA2R cutoff for PA screening was 8.3 (pmol/L)/(pmol/L). We then compared the diagnostic performance of the AA2R with the ARR among 25 patients with PA administered ramipril (5 mg/day) for 2 weeks. Compared with basally, plasma levels of equilibrium angiotensin I (eqAngI) and direct renin concentration increased significantly ( P <0.01 or P <0.05) after ramipril treatment, whereas eqAngII and ACE activity (eqAngII/eqAngI) decreased significantly ( P <0.01). The changes of plasma renin activity and plasma aldosterone concentration in the current study were not significant. On day 14, 4 patients displayed false-negative results using ARR_direct renin concentration (plasma aldosterone concentration/direct renin concentration), 3 of whom also showed false-negative ARR_plasma renin activity (plasma aldosterone concentration/plasma renin activity). On day 15, 2 patients still demonstrated false-negative ARR_plasma renin activity, one of whom also showed a false-negative ARR_direct renin concentration. No false-negative AA2R results were observed on either day 14 or 15. In conclusion, compared with ARR which can be affected by ACE inhibitors causing false-negative screening results, the AA2R seems to be superior in detecting PA among subjects receiving ACE inhibitors.

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