scholarly journals Gender differences renin-angiotensin-aldosterone system and its relation to humoral factors in patients with arterial hypertension

2015 ◽  
Vol 12 (3) ◽  
pp. 34-38
Author(s):  
G M Dadashova

Aim. Explore gender characteristics of the renin-angiotensin-aldosterone system (RAAS), to assess the state of the RAAS relationship with the level of female sex hormones, aldosterone, plasma renin activity in patients with arterial hypertension (AH) in postmenopausal women.Materials and methods. The study included 35 patients with hypertension 1-3-th degree, the average age 56.8±6.9 years. The control group included 21 healthy people with a normal body mass index (BMI). Each of these groups was divided into subgroups by gender: group IA included healthy men (n=10), group IB - healthy women (n=11), group IIA - men with hypertension (n=17), group IIB - Women with hypertension (n=18). Evaluation was carried out with a hormonal status determining levels of estradiol, testosterone, aldosterone, plasma renin activity in the serum.Results. Aldosterone concentration in group IIB was 169.8±109.9 pg/ml and was significantly higher (p

1982 ◽  
Vol 63 (s8) ◽  
pp. 207s-209s ◽  
Author(s):  
Ph. Glasson ◽  
H. Favre ◽  
M. B. Vallotton

1. Chronic ambulatory peritoneal dialysis allows good control of blood pressure in patients with hypertensive end-stage renal disease. The role of the renin-angiotensin-aldosterone system has therefore been studied in seven patients during the first 6 months of chronic ambulatory peritoneal dialysis treatment. 2. Steady increases in plasma renin activity and aldosterone were observed with a good correlation between these two variables. Plasma electrolytes, renin substrate and body weight did not change significantly. 3. Angiotensin II perfusion tests, performed at the end of the study, showed a relative vascular resistance to angiotensin II. 4. Stimulation of the renin-angiotensin-aldosterone system may be partially explained by this last observation or by removal of an unknown vasopressor substance responsible for the inhibition of the plasma renin activity.


1979 ◽  
Vol 57 (s5) ◽  
pp. 145s-148s ◽  
Author(s):  
G. A. MacGregor ◽  
N. D. Markandu ◽  
J. E. Roulston

1. Propranolol, saralasin and captopril changed blood pressure in normotensive as well as hypertensive subjects. 2. The percentage change in blood pressure with these three drugs for a given plasma renin activity was similar in normotensive and hypertensive subjects. 3. This suggests that when the renin-angiotensin system is maintaining blood pressure, it maintains the blood pressure to the same extent in percentage terms in normotensive and hypertensive subjects for a given plasma renin activity. 4. Saralasin has marked agonist activity, and probably underestimates the participation of the renin—angiotensin—aldosterone system in the maintenance of blood pressure. The fall in blood pressure that occurred with captopril in normal subjects on their normal sodium intake suggests that the renin—angiotensin—aldosterone system may have an important role in the control of blood pressure in normal subjects on their normal sodium intake. If it does, our results suggest that the renin—angiotensin—aldosterone system plays no greater role in maintaining blood pressure in patients with essential hypertension than normotensive subjects for a given plasma renin activity.


2018 ◽  
Vol 19 (4) ◽  
pp. 147032031881002 ◽  
Author(s):  
Tomasz Pizoń ◽  
Marek Rajzer ◽  
Wiktoria Wojciechowska ◽  
Małgorzata Wach-Pizoń ◽  
Tomasz Drożdż ◽  
...  

Introduction: The aim of the study was to evaluate clinical and biochemical differences between patients with low-renin and high-renin primary arterial hypertension (AH), mainly in reference to serum lipids, and to identify factors determining lipid concentrations. Materials and methods: In untreated patients with AH stage 1 we measured plasma renin activity (PRA) and subdivided the group into low-renin (PRA < 0.65 ng/mL/h) and high-renin (PRA ⩾ 0.65 ng/mL/h) AH. We compared office and 24-h ambulatory blood pressure, serum aldosterone, lipids and selected biochemical parameters between subgroups. Factors determining lipid concentration in both subgroups were assessed in regression analysis. Results: Patients with high-renin hypertension ( N = 58) were characterized by higher heart rate ( p = 0.04), lower serum sodium ( p < 0.01) and aldosterone-to-renin ratio ( p < 0.01), and significantly higher serum aldosterone ( p = 0.03), albumin ( p < 0.01), total protein ( p < 0.01), total cholesterol ( p = 0.01) and low-density lipoprotein cholesterol (LDL-C) ( p = 0.04) than low-renin subjects ( N = 39). In univariate linear regression, only PRA in the low-renin group was in a positive relationship with LDL-C ( R2 = 0.15, β = 1.53 and p = 0.013); this association remained significant after adjustment for age, sex, and serum albumin and aldosterone concentrations. Conclusions: Higher serum levels of total and LDL-C characterized high-renin subjects, but the association between LDL-C level and PRA existed only in low-renin primary AH.


1983 ◽  
Vol 64 (5) ◽  
pp. 463-470
Author(s):  
Y. Takata ◽  
A. E. Doyle ◽  
M. Veroni ◽  
S. G. Duffy

1. Blood pressure, the hypotensive effect of captopril, plasma renin activity, renal renin content and kidney weight were measured in the two-kidney—one-clip model, the one-kidney—one-clip model and the two-kidney—one-clip model with the ureter of the contralateral kidney ligated in rats. The ureteric ligation was performed to abolish urinary excretion from the contralateral kidney in the two-kidney—one-clip model. 2. The development of hypertension after renal artery constriction was earlier and greater in the one-kidney—one-clip model and the two-kidney—one-clip model with ureter of the contralateral kidney ligated than in the two-kidney—one-clip model. A single oral dose of captopril produced a greater fall in blood pressure in both the two-kidney models than in the one-kidney—one-clip group. 3. Plasma renin activity and renal renin content of the clipped kidney were higher in the two-kidney model rats, whether or not the ureter had been ligated, than in the one-kidney—one-clip model animals, although more than half the rats from the two-kidney model had normal values. There was a significant correlation between plasma renin activity and the response to captopril in all groups, whereas in none of the three groups was the correlation between plasma renin activity and blood pressure significant. 4. The clipped kidney had a higher renin content than did the contralateral kidney, and the weight of the ischaemic kidney was decreased compared with the contralateral kidney whether it was untouched or had its ureter ligated. The weight of the clipped kidney was in the order one-kidney—one-clip model > two-kidney—one-clip model with ureter of the contralateral kidney ligated > two-kidney—one-clip model. 5. It was concluded that the renin-angiotensin system was stimulated to the similar degree in some animals for the two-kidney—one-clip models, whether or not the ureter of the contralateral kidney had been ligated, compared with the one-kidney—one-clip animals. This finding suggests that the contralateral kidney can stimulate renin secretion and synthesis in the clipped kidney independently of Na+ excretion.


1985 ◽  
Vol 59 (3) ◽  
pp. 924-927 ◽  
Author(s):  
P. R. Freund ◽  
G. L. Brengelmann

We recently found that paraplegic humans respond to hyperthermia with subnormal increase in skin blood flow (SkBF), based on measurements of forearm blood flow (FBF). Is this inhibition of SkBF a defect in thermoregulation or a cardiovascular adjustment necessary for blood pressure control? Since high resting plasma renin activity (PRA) is found in unstressed individuals with spinal cord lesions and since PRA increases during hyperthermia in normal humans, we inquired whether the renin-angiotensin system is responsible for the attenuated FBF in hyperthermic resting paraplegics. Five subjects, 28–47 yr, with spinal transections (T1-T10), were heated in water-perfused suits. Blood samples for PRA determinations were collected during a control period and after internal temperature reached approximately 38 degrees C. Some subjects with markedly attenuated FBF had little or no elevation of PRA; those with the best-developed FBF response exhibited the highest PRA. Clearly, circulating angiotensin is not the agent that attenuates SkBF. Rather, increased activity of the renin-angiotensin system may be a favorable adaptation that counters the locally mediated SkBF increase in the lower body and thus allows controlled active vasodilation in the part of the body subject to centrally integrated sympathetic effector outflow.


2017 ◽  
Vol 18 (3) ◽  
pp. 147032031772991 ◽  
Author(s):  
Petra Nijst ◽  
Frederik H Verbrugge ◽  
Pieter Martens ◽  
Philippe B Bertrand ◽  
Matthias Dupont ◽  
...  

Background: Renin-angiotensin-aldosterone system (RAAS) activation in heart failure with reduced ejection fraction (HFREF) is detrimental through promotion of ventricular remodeling and salt and water retention. Aims: The aims of this article are to describe RAAS activity in distinct HFREF populations and to assess its prognostic impact. Methods: Venous blood samples were prospectively obtained in 76 healthy volunteers, 72 patients hospitalized for acute decompensated HFREF, and 78 ambulatory chronic HFREF patients without clinical signs of congestion. Sequential measurements were performed in patients with acute decompensated HFREF. Results: Plasma renin activity (PRA) was significantly higher in ambulatory chronic HFREF (7.6 ng/ml/h (2.2; 18.1)) compared to patients with acute decompensated HFREF (1.5 ng/ml/h (0.8; 5.7)) or healthy volunteers (1.4 ng/ml/h (0.6; 2.3)) (all p < 0.05). PRA was significantly associated with arterial blood pressure and renin-angiotensin system blocker dose. A progressive rise in PRA (+4 ng/ml/h (0.4; 10.9); p < 0.001) was observed in acute decompensated HFREF patients after three consecutive days of decongestive treatment. Only in acute HFREF were PRA levels associated with increased cardiovascular mortality or HF readmissions ( p = 0.035). Conclusion: PRA is significantly elevated in ambulatory chronic HFREF patients but is not associated with worse outcome. In contrast, in acute HFREF patients, PRA is associated with cardiovascular mortality or HF readmissions.


1996 ◽  
Vol 135 (2) ◽  
pp. 238-244 ◽  
Author(s):  
Micheline Gourmelen ◽  
Irène Saint-Jacques ◽  
Gilles Morineau ◽  
Hany Soliman ◽  
René Julien ◽  
...  

Gourmelen M. Saint-Jacques I, Morineau G. Soliman H, Julien R, Fiet J. 11β-Hydroxysteroid dehydrogenase deficit: a rare cause of arterial hypertension. Diagnosis and therapeutic approach in two young brothers. Eur J Endocrinol 1996;135:238–44. ISSN 0804–4643 We report the clinical history and results of endocrine investigations in two brothers born to consanguineous parents, who presented with hypokalemia and arterial hypertension when they were aged 2 and 6 years. The hormonal serum assay results, including extremely low values for aldosterone and plasma renin activity, favored the existence of apparent mineralocorticoid excess. A diagnosis of 11β-hydroxysteroid dehydrogenase (11β-HSD) deficiency was made, based on assays of the hydrogenated urinary metabolites of cortisol and cortisone, as well as of corticosterone and dehydrocorticosterone. Indeed we found a very low rate of urinary elimination of cortisone metabolites: tetrahydrogenated cortisone was reduced to between 0.10 and 30 μmol/24 h, which is 15–100 times lower than the normal rate; hexahydrogenated cortolones a and β were found to be 7-to 20-fold lower than normal levels; and the 11-keto-17-ketosteroid derivatives of cortisone were also reduced. Urinary elimination of the cortisol-reduced metabolites 5β- and 5α-tetrahydrogenated cortisol were slightly reduced or normal. These results argue in favor of a deficit in the enzyme 11β-HSD, which oxidizes cortisol into cortisone. A moderate defect in the conversion of cortisol into 5β-THF compared to normal conversion into 5α-THF was also found. With respect to corticosterone metabolism, we demonstrated the presence of a defect in the oxidation of that steroid into dehydrocorticosterone, also due to the deficit in 11β-HSD. Arterial hypertension and hypokalemia were corrected by treatment with dexamethasone, concomitantly with correction of the low aldosterone and plasma renin activity levels. On the other hand, during this treatment, urinary concentrations of the metabolites of cortisol. cortisone and corticosterone were only moderately affected. Jean Fiet, Laboratoire de Biologie Hormonale, Hôpital Saint-Louis, I Avenue Claude Vellefaux, 75475 Paris Cedex 10, France


1980 ◽  
Vol 59 (s6) ◽  
pp. 101s-103s ◽  
Author(s):  
J. R. Sowers ◽  
M. L. Tuck ◽  
J. Barrett ◽  
M. P. Sambhi ◽  
M. S. Golub

1. In rats, intra-arterial metoclopramide, a dopamine antagonist, resulted in an elevation of plasma aldosterone at 5 min and plasma renin activity at 10 min and peak aldosterone and renin responses at 10 and 30 min respectively. 2. Pre-administration of l-dopa blunted and delayed aldosterone and renin responses to metoclopramide, indicating that metoclopramide-induced plasma aldosterone and plasma renin activity increments are mediated by a direct effect of blockade of dopamine receptors rather than other effects of this drug. 3. Pre-administration of angiotensin converting enzyme inhibitor, captopril (SQ 14 225) and the angiotensin II antagonist, saralasin, as well as bilateral nephrectomy did not significantly affect the aldosterone response to metoclopramide, Thus dopaminergic modulation of aldosterone secretion occurs independently of alterations in the renin-angiotensin system. 4. Modulating effects of dopamine on plasma aldosterone are probably mediated by direct effects as well as by interaction with other factors influencing aldosterone secretion at the adrenal zona glomerulosa.


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