Acromegaly and hypertension: role of the renin-angiotensin-aldosterone system

1982 ◽  
Vol 100 (4) ◽  
pp. 581-587 ◽  
Author(s):  
Bengt E. Karlberg ◽  
Anna-Maria Ottosson
Keyword(s):  
Blood Pressure ◽  
High Frequency ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Substantial Part ◽  
Volume Factor ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Before And After

Abstract. The incidence of arterial hypertension was evaluated in a partly retrospective study of patients with active acromegaly. Of 37 patients studied, 18 (48%) had hypertension, i.e. a supine blood pressure of > 160/95 mmHg. The type of hypertension was explored further by measuring plasma renin activity and, in some patients plasma aldosterone concentrations before and after stimulation (upright posture or furosemide 80 mg given orally). Urinary 24 h excretion of aldosterone was also determined. About half of the patients with hypertension but also a substantial part of normotensive acromegalics had inappropriately low plasma renin levels both during basal conditions and after stimulation. On the other hand urinary aldosterone excretion was either normal or (in 2 patients) slightly elevated. There was no other evidence of coexistent primary aldosteronism. Our results confirm previous reports of a high frequency of alterations in the renin-angiotensin-aldosterone system in acromegalic patients with growth hormone excess which in some instances may lead to an elevated blood pressure. The biochemical changes have many similarities to low renin essential hypertension. A volume factor may be operating in acromegalic patients with hypertension since in 10 patients treatment with the aldosterone antagonist, spironolactone, with doses between 50–200 mg daily lowered blood pressure to near normal levels. Thus, spironolactone seems to be a worthwhile alternative in the treatment of hypertensive acromegalics.

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.

scholarly journals Role of renin-angiotensin-aldosterone system in salt-sensitive hypertension induced by sensory denervation

2001 ◽  
Vol 281 (5) ◽  
pp. H2143-H2149 ◽  
Author(s):  
Yan Huang ◽  
Donna H. Wang
Keyword(s):  
Blood Pressure ◽  
Plasma Renin ◽  
Male Rats ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
High Sodium ◽  
Sodium Diet ◽  
Sensory Denervation ◽  
Salt Sensitive Hypertension

To define the role of the renin-angiotensin-aldosterone system in a novel salt-sensitive model, neonatal Wistar rats were given capsaicin (50 mg/kg sc) on the first and second days of life. After weaning, male rats were divided into the following six groups and treated for 3 wk with: control + normal sodium diet (CON-NS), CON + high-sodium diet (CON-HS), CON + HS + spironolactone (50 mg · kg−1 · day−1, CON-HS-SP), capsaicin pretreatment + NS (CAP-NS), CAP-HS, and CAP-HS-SP. Radioimmunoassay shows that plasma renin activity (PRA) and plasma aldosterone level (PAL) were suppressed by HS, but they were higher in CAP-HS than in CON-HS and CON-HS-SP ( P < 0.05). Both tail-cuff systolic blood pressure and mean arterial pressure were higher in CAP-HS than in all other groups ( P < 0.05). Urine water and sodium excretion were increased with HS intake, but they were lower in CAP-HS than in CON-HS ( P < 0.05). Western blot did not detect differences in adrenal AT1 receptor content. Therefore, insufficiently suppressed PRA and PAL in response to HS intake by sensory denervation may contribute to increased salt sensitivity and account for effectiveness of spironolactone in lowering blood pressure in this model.

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.

Role of renin-angiotensin system in glucocorticoid hypertension in rats

1982 ◽  
Vol 243 (1) ◽  
pp. E48-E51 ◽  
Author(s):  
H. Suzuki ◽  
M. Handa ◽  
K. Kondo ◽  
T. Saruta
Keyword(s):  
Blood Pressure ◽  
Intravenous Injection ◽  
Enzyme Inhibitor ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Dependent Manner ◽  
Concurrent Administration ◽  
Angiotensin System ◽  
Renin Angiotensin

The role of the renin-angiotensin system in the regulation of the blood pressure of dexamethasone-treated rats (Dex) was evaluated using saralasin, an angiotensin II antagonist, and SQ 14225 (SQ) (d-3-mercapto-2-methylpropranoyl-1-proline), an angiotensin-converting enzyme inhibitor. During a 7-day period blood pressure rose 65 +/- 10 mmHg (P less than 0.001) in Dex with no significant changes in plasma renin activity. Concurrent administration of dexamethasone and SQ attenuated the elevation of blood pressure (P less than 0.05). In the conscious, freely moving state, intravenous injection of SQ (10, 30, 100 micrograms/kg) reduced blood pressure of DEX in a dose-dependent manner (P less than 0.05). Also, intravenous injection of saralasin (10 micrograms.kg-1 . min-1) reduced blood pressure significantly (P less than 0.01). Bilateral nephrectomy abolished the effects of saralasin and SQ on blood pressure in Dex. These results indicate that the elevation of blood pressure in DEX depends partially on the renin-angiotensin system.

scholarly journals Effect of renal denervation on catecholamines and the renin–angiotensin–aldosterone system

2020 ◽  
Vol 21 (3) ◽  
pp. 147032032094309
Author(s):  
Lida Feyz ◽  
Sjoerd van den Berg ◽  
Robert Zietse ◽  
Isabella Kardys ◽  
Jorie Versmissen ◽  
...  
Keyword(s):  
Plasma Renin ◽  
Drug Regimen ◽  
Plasma Aldosterone ◽  
Renal Sympathetic Denervation ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Post Procedure ◽  
Endogenous Catecholamines ◽  
Significant Change ◽  
Renal Sympathetic

Introduction: The effect of renal sympathetic denervation (RDN) on neurohormonal responses is largely unknown. We aimed to assess the effect of RDN on the renin–angiotensin–aldosterone system (RAAS) and endogenous catecholamines. Methods: A total of 60 patients with hypertension underwent RDN and remained on a stable antihypertensive drug regimen. Samples for plasma aldosterone, plasma renin and urine (nor)metanephrine were collected at baseline and at 6 months post procedure. Ambulatory blood pressure (BP) recordings were obtained at baseline and at 6 months post procedure. Results: Mean age was 64±9 years, and 30/60 patients were male. At 6 months, average daytime systolic and diastolic ambulatory BP decreased by 10 and 6 mmHg, respectively ( p<0.001). No significant change was observed in plasma aldosterone (median=248.0 pmol/L (interquartile range (IQR) 113.3–369.5 pmol/L) vs. median=233.0 pmol/L (IQR 110.3–360.8 pmol/L); p=0.66); renin (median=19.5 µIU/mL (IQR 6.8–119.5 µIU/mL) vs. median=14.3 µIU/mL (IQR 7.2–58.0 µIU/mL); p=0.32), urine metanephrine (median=0.46 µmol/L (IQR 0.24–0.77 µmol/L) vs. median=0.46 µmol/L (IQR 0.22–0.88 µmol/L); p=0.75) and normetanephrine (median=1.41 µmol/L (IQR 0.93–2.00 µmol/L vs. median =1.56 (IQR 0.74–2.50 µmol/L); p=0.58) between baseline and 6 months, respectively. No correlation was found between the decrease in mean systolic daytime BP and changes in RAAS hormones or endogenous catecholamines. Conclusion: Despite significant reductions in ambulatory BP, RDN did not result in a significant change in endogenous catecholamines or in RAAS hormones at 6 months.

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 Relationship between the expression of angiotensin II receptors type 1 and vasoactive regulators in arterial hypertension

2020 ◽  
Vol 11 (3) ◽  
pp. 16-21
Author(s):  
Anna V. Logatkina ◽  
Viktor S. Nikiforov ◽  
Stanislav S. Bondar' ◽  
Igor' V. Terekhov ◽  
Vladimir K. Parfeniuk
Keyword(s):  
Blood Pressure ◽  
Arterial Hypertension ◽  
Ace Inhibitor ◽  
High Expression ◽  
Soluble Form ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Low Expression

In the pathogenesis of arterial hypertension (AH), the renin-angiotensin-aldosterone system plays a key role in helping to maintain elevated blood pressure. At the same time, the state of angiotensin-II production (AT II) and the expression level of its receptors on target cells determine the formation of most of the effects underlying the pathogenesis of associated clinical conditions in such patients. Thus, the study of the pathogenesis of AH, namely the study of the role of the AT II axis, the AT II receptor, is an actual scientific and practical task. Aim. Given the important role of type 1 receptors for AT II in the formation of pathological changes in arterial hypertension, the purpose of this study was to study the peculiarities of the effect of their expression on biochemical processes in patients with arterial hypertension. Material and methods. In the course of the clinical study, 60 patients of both sexes with hypertension aged 45 to 55 years old were admitted to the clinic for planned treatment. Depending on the initial level of expression of receptors for AT II (AT1R), determined by the serum concentration of the soluble form of type 1 receptors for AT II, the patients were divided into two subgroups with conditionally low (corresponding to the concentration of the soluble form of the receptor for AT II 0.66 ng/ml) and conditionally high (1.57 ng/ml) expression. The analysis showed that high expression of AT1R is associated with elevated plasma levels of renin by 30.8% (p=0.0005), AT II by 48.1% (p=0.00001), E-selectin by 47.9% (p=0.0001), VCAM-1 by 29.1% (p=0.00001), ICAM-1 by 52.9% (p=0.00001), VE-cadherin by 50.9% (p=0.00001), endothelin-1 by 48.8% (p=0.0005), an ACE inhibitor by 13.6% (p=0.047), and CRP by 74.1% (p=0.00002 ) and endoperoxide by 29.7% (p=0.009). Against this background, there was a decrease in the level of apoA1 by 21.6% (p=0.027), ACE by 20.1% (p=0.1), the level of antioxidants by 22.3% (p=0.00001). The analysis showed that in the group with initially high expression of AT1R, there was an increased blood pressure, the level of which, on average, exceeded the values of patients with low expression of the indicated receptor by 24.5 mm Hg (p=0.011). Against the background of therapy in the group with high expression of AT1R, plasma renin activity decreased by 20.3% (p=0.013), endoperoxide by 8.4% (p=0.038), an ACE inhibitor by 14.6% (p=0.02). At the same time, the level of apoA1 increased by 8.5% (p=0.036), antioxidants by 8.6% (p=0.036), ICAM-1 by 5.3% (p=0.05), VE-cadherin by 2.5% (p=0.07). The level of the remaining factors was not statistically significant. In the subgroup with low expression of the AT II receptor, during treatment, there was a decrease in endoperoxide by 12.8% (p=0.031), an ACE inhibitor by 5.5% (p=0.044) without significant changes in other indicators. Conclusion. In hypertensive patients, higher expression of AT1R is associated with high activation of immune-inflammatory mechanisms, dyslipidemia, an imbalance of the lipid peroxidation system and antioxidant protection, as well as higher renin-angiotensin-aldosterone system activity and increased arterial pressure. On the background of antihypertensive therapy, partial compensation of the identified changes is achieved, including a moderate increase in the level of antioxidants, a decrease in the concentration of endoperoxide, renin activity and an increase in the level of apoA1, while maintaining an increased level of AT II, high expression of receptors to it. These changes indicate the need for further search for effective antihypertensive therapy strategies aimed at limiting the activity of renin-angiotensin-aldosterone system in patients with hypertension.

scholarly journals Role of the Renin-Angiotensin-Aldosterone System in Various Disease Processes: An Overview

2021 ◽  
Author(s):  
Volkan Gelen ◽  
Abdulsamed Kükürt ◽  
Emin Şengül
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Electrolyte Balance ◽  
Physiological System ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Working Principle ◽  
Kidney Liver ◽  
Regulation Of Blood Pressure

The renin-angiotensin-aldosterone system is a physiological system that plays an important role in the regulation of blood pressure and body water-electrolyte balance, in which the kidney, liver and lungs play a role in its activation. This system comes into play in various diseases such as the cardiovascular, renal, pulmonary and nervous system where blood pressure and fluid-electrolyte balance may change. The purpose of this study, which is presented in line with this information, is to explain the working principle of this system, how this system is activated, how it comes into play in the mentioned diseases, and what kind of results occur.

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