scholarly journals Plasma renin activity, serum aldosterone concentration and selected organ damage indices in essential arterial hypertension

2021 ◽  
Vol 17 (1) ◽  
pp. 9-18
Author(s):  
Tomasz Pizoń ◽  
Marek Rajzer ◽  
Wiktoria Wojciechowska ◽  
Tomasz Drożdż ◽  
Dorota Drożdż ◽  
...  
Keyword(s):  
Plasma Renin Activity ◽  
Arterial Hypertension ◽  
Plasma Renin ◽  
Organ Damage ◽  
Renin Activity ◽  
Plasma Sodium ◽  
Damage Indices ◽  
Serum Aldosterone ◽  
Lower Egfr ◽  
Aldosterone To Renin Ratio

IntroductionThe aim of this study was to assess the relations between plasma renin activity (PRA), serum aldosterone concentration (ALDO) and selected asymptomatic organ damage (AOD) indices in mild primary arterial hypertension (AH).Material and MethodsWe measured PRA, ALDO, and selected AOD indices (carotid-femoral pulse wave velocity (cfPWV), central aortic pulse pressure (cPP), estimated glomerular filtration rate (eGFR)) in 122 patients with untreated AH.ResultsPatients with high PRA (≥ 0.65 ng/ml/h) were characterized by lower plasma sodium and aldosterone to renin ratio (ARR), higher ALDO, but a similar level of AOD indices compared to patients with low PRA. cfPWV (p = 0.04) and cPP (p = 0.019) increased with ARR, while eGFR decreased with ALDO (p = 0.008). Only eGFR was independently correlated with ALDO. In subjects with simultaneously high PRA and ARR values, we found significantly higher cfPWV (p = 0.02) and cPP (p = 0.04) and lower eGFR (p = 0.02) than in those with high PRA but low ARR values.ConclusionsAssessment of the influence of the renin-angiotensin-aldosterone system (RAAS) on AOD should include the relationship between renin and aldosterone. The PRA itself has no predictive value for AOD. More advanced arterial stiffness and renal impairment are associated with increased PRA and ARR. The RAAS activity might be useful in AOD prediction and hypertension severity assessment.

scholarly journals The relationship between plasma renin activity and serum lipid profiles in patients with primary arterial hypertension

2018 ◽  
Vol 19 (4) ◽  
pp. 147032031881002 ◽  
Author(s):  
Tomasz Pizoń ◽  
Marek Rajzer ◽  
Wiktoria Wojciechowska ◽  
Małgorzata Wach-Pizoń ◽  
Tomasz Drożdż ◽  
...  
Keyword(s):  
Plasma Renin Activity ◽  
Arterial Hypertension ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Plasma Renin ◽  
Serum Levels ◽  
Renin Activity ◽  
Serum Aldosterone ◽  
Primary Arterial Hypertension ◽  
Aldosterone To Renin Ratio

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.

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.

Plasma renin activity and serum aldosterone during prolonged physical strain

1985 ◽  
Vol 54 (1) ◽  
pp. 1-6 ◽  
Author(s):  
P. K. Opstad ◽  
O. �ktedalen ◽  
A. Aakvaag ◽  
F. Fonnum ◽  
P. K. Lund
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Physical Strain ◽  
Serum Aldosterone

11β-Hydroxysteroid dehydrogenase deficit: a rare cause of arterial hypertension. Diagnosis and therapeutic approach in two young brothers

1996 ◽  
Vol 135 (2) ◽  
pp. 238-244 ◽  
Author(s):  
Micheline Gourmelen ◽  
Irène Saint-Jacques ◽  
Gilles Morineau ◽  
Hany Soliman ◽  
René Julien ◽  
...  
Keyword(s):  
Plasma Renin Activity ◽  
Arterial Hypertension ◽  
Therapeutic Approach ◽  
Plasma Renin ◽  
Clinical History ◽  
Hydroxysteroid Dehydrogenase ◽  
Renin Activity ◽  
Activity Levels ◽  
Urinary Elimination ◽  
Hypertension Diagnosis

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

Effect of Chronic Low-Dose Arginine Vasopressin Infusion on Body Fluid Homoeostasis during Adaptation from a High-to a Low-Sodium Diet in Normal Man

1993 ◽  
Vol 85 (4) ◽  
pp. 465-470 ◽  
Author(s):  
M. Sutters ◽  
D. J. S. Carmichael ◽  
S. L. Lightman ◽  
W. S. Peart
Keyword(s):  
Plasma Renin Activity ◽  
Arginine Vasopressin ◽  
Plasma Renin ◽  
Sodium Concentration ◽  
Renin Activity ◽  
Plasma Sodium ◽  
Angiotensin I ◽  
Salt Restriction ◽  
Plasma Sodium Concentration ◽  
Plasma Arginine

1. A diuresis occurs within the first 36 h of salt restriction. A decline in plasma arginine vasopressin concentration may contribute to both the diuresis and antinatriuresis. 2. We have studied six normal human subjects during 36 h of dietary sodium restriction. In one study subjects received an intravenous infusion of D-glucose, and in the other an infusion of arginine vasopressin (6 fmol min−1 kg−1). 3. In the D-glucose phase plasma arginine vasopressin concentration fell (1.77 +034 to 1.02 +0.13 pg/ml), urine flow increased (67.9 +113 to 89.8 + 17.1 ml/h), haemoconcentration occurred (packed cell volume 40.8 +0.3 to 42.8 +03%, protein concentration 71.6 +03 to 74.5 + 0.6 g/l), plasma sodium concentration fell (140 +0.2 to 138 +0.2 mmol/l) and plasma renin activity increased (1600+153 to 3700 + 356 pg of angiotensin I h−1 ml−1). 4. In the arginine vasopressin phase plasma arginine vasopressin concentration remained constant (13 + 0.13 to 134 +0.11 pg/ml), the diuresis was reversed (65.7 +9.9 to 52.1 +8.9 ml/h), plasma sodium concentration fell further (139.8 +0.4 to 136.1 +0.4 mmol/l), the rise in plasma renin activity was reduced (arginine vasopressin 2552 + 292; D-glucose, 3700 + 356 pg of angiotensin I h−1 ml−1) and creatinine clearance was lower in the last 12 h of salt restriction (arginine vasopressin, 96.1 +6.9; D-glucose 116.5 + 6.8 ml/min). Renal sodium excretion was unaffected by arginine vasopressin infusion. 5. We conclude that the fall in plasma arginine vasopressin concentration during dietary salt restriction, whilst not affecting renal sodium excretion, may be important in the regulation of plasma sodium concentration, plasma renin activity and glomerular filtration.

Effect of an opiate antagonist on the responses of circulating catecholamines and the renin-aldosterone system to acute sympathetic stimulation by hand-grip in man

1986 ◽  
Vol 111 (2) ◽  
pp. 252-257 ◽  
Author(s):  
K. S. L. Lam ◽  
A. Grossman ◽  
P. Bouloux ◽  
P. L. Drury ◽  
G. M. Besser
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Endogenous Opioids ◽  
Renin Activity ◽  
Mild Stress ◽  
Sympathetic Stimulation ◽  
Plasma Adrenaline ◽  
Hand Grip ◽  
Serum Aldosterone

Abstract. The effect of naloxone on the neurohumoral responses to acute sympathetic stimulation by sustained hand-grip in normal man was investigated. Six normal males were studied fasting at 08.30 h, on two occasions at 7-day intervals, with each subject sustaining 30% of his maximal hand-grip on a hand dynamometer for 5 min. Naloxone (8 mg bolus) in 20 ml normal saline, or saline alone, was given 5 min before hand-grip in a randomised double-blind cross-over trial. Blood was sampled for plasma renin activity, serum aldosterone and plasma catecholamines. The study was repeated in the absence of hand-grip. Sustained hand-grip produced significant elevations in mean blood-pressure, circulating adrenaline, noradrenaline and aldosterone. Naloxone, which had no effect on basal catecholamines, plasma renin activity or aldosterone, significantly enhanced the responses in plasma adrenaline, plasma renin activity and serum aldosterone to hand-grip. The increments in blood pressure and noradrenaline were not affected. These results suggest that endogenous opioids modulate the response of the sympathoadrenal and renin-aldosterone systems to acute sympathetic stimulation by a mild stress in man.

scholarly journals SUN-189 A Case of Delayed Hypoaldosteronism Following Unilateral Adrenalectomy for Primary Aldosteronism

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Julie Schommer ◽  
Amal A Shibli-Rahhal
Keyword(s):  
Adrenal Gland ◽  
Plasma Renin Activity ◽  
Potassium Chloride ◽  
Primary Aldosteronism ◽  
Plasma Renin ◽  
Renin Activity ◽  
Endocrine Society ◽  
Unilateral Adrenalectomy ◽  
One Year ◽  
Aldosterone To Renin Ratio

Abstract BACKGROUND: Hypoaldosteronism occurs in 6–30% of patients following unilateral adrenalectomy for primary aldosteronism. The Endocrine Society guidelines recommend discontinuing potassium supplementation and spironolactone postoperatively with repeat renin and aldosterone after surgery to monitor for cure. Clinical Case: A 69-year-old male with a 15-year history of hypertension on amlodipine 10 mg daily, atenolol 100 mg daily, terazosin 5 mg daily, valsartan 160 mg daily, spironolactone 50 mg three times daily, with longstanding hypokalemia on potassium chloride 20 mEq four times daily presented with an ischemic stroke and persistent hypertension (BP 182/79). Following discontinuation of spironolactone, evaluation revealed aldosterone concentration of 214 ng/dL (normal 4.0 - 31) and plasma renin activity of 0.1 ng/mL/hr (normal 0.5 - 4.0), giving an aldosterone-to-renin ratio of 2,140. CT of the abdomen showed a 3 cm right adrenal mass. He underwent uncomplicated right adrenalectomy for primary aldosteronism. Postoperative potassium was 3.4 mEq/L (normal 3.5–5.0) and hypertension persisted, so he was discharged on potassium chloride 10 mEq, losartan 100 mg daily, amlodipine 10 mg daily, and labetalol 200 mg twice daily. Two weeks later potassium level was 5.1 mEq/L and potassium chloride supplement was discontinued. Six months postoperatively, potassium was 5.7 mEq/L with well-controlled blood pressure, so losartan was discontinued. Labs over the subsequent several weeks showed persistent hyperkalemia up to 6.2 mEq/L and new hyponatremia to 128 mEq/L (normal 134 - 150). Repeat plasma renin activity was 0.51 ng/mL/hr and aldosterone concentration &lt;1.0 ng/dL. Morning cortisol concentration was 18.3 ug/dL (normal 6.7 - 22.6) and ACTH 38 pg/mL (normal 6.0 - 50 pg/mL). He was diagnosed with postsurgical hypoaldosteronism. Potassium stabilized at 5.1 mEq/L and sodium stabilized at 134 mEq/L, so he was monitored without treatment for hypoaldosteronism. One year postoperatively his labs showed: potassium 5.1 mEq/L, sodium 135 mEq/L, renin 1.0 ng/mL/hr, and aldosterone 5.7 ng/dL. Conclusion: This patient had primary aldosteronism leading to suppression of aldosterone secretion from the contralateral healthy adrenal gland. This resulted in postoperative hypoaldosteronism once the affected adrenal gland was resected. This case demonstrates the need for continued monitoring of potassium, sodium, renin, and aldosterone following unilateral adrenalectomy for primary aldosteronism, especially in the setting of postoperative angiotensin receptor blocker use or other medications which can affect the renin-angiotensin-aldosterone system.

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