scholarly journals Blood Pressure Goal Attainment: Meeting the Challenge of the JNC 7's Blood Pressure Goals and the Role of Renin‐Angiotensin‐Aldosterone System Blockade

2004 ◽  
Vol 6 (12) ◽  
pp. 699-705 ◽  
Author(s):  
Michael Weber ◽  
Jan Basile ◽  
Joseph Izzo ◽  
Suzanne Oparil
1982 ◽  
Vol 100 (4) ◽  
pp. 581-587 ◽  
Author(s):  
Bengt E. Karlberg ◽  
Anna-Maria Ottosson

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.


2020 ◽  
Vol 11 (3) ◽  
pp. 16-21
Author(s):  
Anna V. Logatkina ◽  
Viktor S. Nikiforov ◽  
Stanislav S. Bondar' ◽  
Igor' V. Terekhov ◽  
Vladimir K. Parfeniuk

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.


2021 ◽  
Author(s):  
Volkan Gelen ◽  
Abdulsamed Kükürt ◽  
Emin Şengül

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.


2017 ◽  
Vol 312 (3) ◽  
pp. H437-H445 ◽  
Author(s):  
Rafael L. Morais ◽  
Aline M. Hilzendeger ◽  
Bruna Visniauskas ◽  
Mihail Todiras ◽  
Natalia Alenina ◽  
...  

Obesity is assumed to be a major cause of human essential hypertension; however, the mechanisms responsible for weight-related increase in blood pressure (BP) are not fully understood. The prevalence of hypertension induced by obesity has grown over the years, and the role of the renin-angiotensin-aldosterone system (RAAS) in this process continues to be elucidated. In this scenario, the ob/ob mice are a genetic obesity model generally used for metabolic disorder studies. These mice are normotensive even though they present several metabolic conditions that predispose them to hypertension. Although the normotensive trait in these mice is associated with the poor activation of sympathetic nervous system by the lack of leptin, we demonstrated that ob/ob mice present massively increased aminopeptidase A (APA) activity in the circulation. APA enzyme metabolizes angiotensin (ANG) II into ANG III, a peptide associated with intrarenal angiotensin type 2 (AT2) receptor activation and induction of natriuresis. In these mice, we found increased ANG-III levels in the circulation, high AT2 receptor expression in the kidney, and enhanced natriuresis. AT2 receptor blocking and APA inhibition increased BP, suggesting the ANG III-AT2 receptor axis as a complementary BP control mechanism. Circulating APA activity was significantly reduced by weight loss independently of leptin, indicating the role of fat tissue in APA production. Therefore, in this study we provide new data supporting the role of APA in BP control in ob/ob mouse strain. These findings improve our comprehension about obesity-related hypertension and suggest new tools for its treatment. NEW & NOTEWORTHY In this study, we reported an increased angiotensin III generation in the circulation of ob/ob mice caused by a high aminopeptidase A activity. These findings are associated with an increased natriuresis found in these mice and support the role of renin-angiotensin-aldosterone system as additional mechanism regulating blood pressure in this genetic obese strain.


Molecules ◽  
2021 ◽  
Vol 26 (6) ◽  
pp. 1523
Author(s):  
Anna Pierzchlińska ◽  
Magdalena Kwaśniak-Butowska ◽  
Jarosław Sławek ◽  
Marek Droździk ◽  
Monika Białecka

Dementia is one of the most disabling non-motor symptoms in Parkinson’s disease (PD). Unlike in Alzheimer’s disease, the vascular pathology in PD is less documented. Due to the uncertain role of commonly investigated metabolic or vascular factors, e.g., hypertension or diabetes, other factors corresponding to PD dementia have been proposed. Associated dysautonomia and dopaminergic treatment seem to have an impact on diurnal blood pressure (BP) variability, which may presumably contribute to white matter hyperintensities (WMH) development and cognitive decline. We aim to review possible vascular and metabolic factors: Renin-angiotensin-aldosterone system, vascular endothelial growth factor (VEGF), hyperhomocysteinemia (HHcy), as well as the dopaminergic treatment, in the etiopathogenesis of PD dementia. Additionally, we focus on the role of polymorphisms within the genes for catechol-O-methyltransferase (COMT), apolipoprotein E (APOE), vascular endothelial growth factor (VEGF), and for renin-angiotensin-aldosterone system components, and their contribution to cognitive decline in PD. Determining vascular risk factors and their contribution to the cognitive impairment in PD may result in screening, as well as preventive measures.


2001 ◽  
Vol 281 (5) ◽  
pp. H2143-H2149 ◽  
Author(s):  
Yan Huang ◽  
Donna H. Wang

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.


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