scholarly journals Effect of the Renin-Angiotensin-Aldosterone System Reactivity on Endothelial Function and Modulative Role of Valsartan in Male Subjects with Essential Hypertension

2021 ◽  
Vol 10 (24) ◽  
pp. 5816
Author(s):  
Jakub Jasiczek ◽  
Małgorzata Trocha ◽  
Arkadiusz Derkacz ◽  
Ewa Szahidewicz-Krupska ◽  
Adrian Doroszko
Keyword(s):  
Endothelial Function ◽  
Plasma Renin ◽  
Blood Concentrations ◽  
Renin Angiotensin ◽  
Stress Markers ◽  
No Bioavailability ◽  
Flow Mediated Vasodilation ◽  
Male Subjects ◽  
Pai 1

Background: The aim of the study was to evaluate the relationship between renin-angiotensin-aldosterone (RAA) system activity and reactivity, and the endothelial function profile in normotensive subjects (N), and in essential hypertensives (H), followed by analysis of the modulatory role of an angiotensin receptor blocker (ARB): valsartan, administered in the management of hypertension. Methods: A total of 101 male subjects were enrolled to the study: 31H and 70N. The nitric-oxide (NO) bioavailability (l-Arginine, asymmetric dimethylarginine (ADMA)), symmetric dimethylarginine (SDMA), endothelial vasodilative function (flow mediated dilation (FMD)), oxidative-stress markers (malonyldialdehyde (MDA), thiol index (GSH/GSSG), nitrotyrozine (N-Tyr)), and pro-inflammatory/angiogenic parameters (sICAM-1, sVCAM-1, PAI-1, sE-selectin, PAI-1, thromboxane -B2) were assessed at baseline, then after intravenous -l-arginine administration, which was repeated after the 4-day acetylsalicylic acid (ASA) administration (75 mg/24 h). In hypertensives, this whole protocol was repeated following 2 weeks of valsartan therapy. Results: No effect of valsartan and ASA on the flow-mediated vasodilation (FMD) and the NO bioavailability in hypertensives was observed. Administration of valsartan increased plasma renin activity (PRA), but without a decrease in the aldosterone levels. ASA treatment minimized the pre-existing differences between the groups, and increased the PRA in the N-subgroup with the highest ARR values. The blood concentrations of proinflammatory sICAM-1, sE-selectin, sVCAM-1, and PAI-1 were higher, whereas the anti-inflammatory 6-keto-PGF1 alpha level was lower in hypertensive subjects. The levels of angiogenic VEGF did not differ between groups. Conclusions: Our study does not confirm the modulative effect of valsartan on endothelial function. Normotensive men showed an increase in FMD after l-arginine administration, possibly indicating baseline impairment of the NO synthesis.

The Renin Angiotensin System and Bipolar Disorder: A Systematic Review

2020 ◽  
Vol 27 (6) ◽  
pp. 520-528 ◽  
Author(s):  
Izabela Guimarães Barbosa ◽  
Giulia Campos Ferreira ◽  
Diomildo Ferreira Andrade Júnior ◽  
Cássio Rocha Januário ◽  
André Rolim Belisário ◽  
...  
Keyword(s):  
Systematic Review ◽  
Bipolar Disorder ◽  
Cardiovascular Diseases ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Angiotensin Receptors ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Search Terms

Bipolar Disorder (BD) is a chronic a multifactorial psychiatric illness that affects mood, cognition, and functioning. BD is associated with several psychiatric conditions as well clinical comorbidities, particularly cardiovascular diseases. The neurobiology of BD is complex and multifactorial and several systems have been implicated. Considering that the Renin Angiotensin System (RAS) plays an important role in cardiovascular diseases and that recently evidence has suggested its role in psychiatric disorders, the aim of the present study is to summarize and to discuss recent findings related to the modulation of RAS components in BD. A systematic search of the literature using the electronic databases MEDLINE and LILACS was conducted through March 2019. The search terms were: “Bipolar Disorder”; “Renin Angiotensin System”; “Angiotensin 2”; “Angiotensin receptors”; “Angiotensin 1-7”; “ACE”; “ACE2”; “Mas Receptor”. We included original studies assessing RAS in BD patients. Two hundred twenty-two citations were initially retrieved. Eleven studies were included in our systematic review. In the majority of studies (6 of 8), the ACE insertion/deletion (I/D) polymorphism did not differ between BD patients and controls. BD patients presented higher plasma renin activity in comparison with controls. The studies evaluating the RAS molecules in BD are very scarce and heterogeneous. The literature suggests a potential role of RAS in BD. Further studies are necessary to investigate this relationship.

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.

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.

The Profile of Endothelial Function in Children with ALL Is Associated with the Risk Stratification Determining the Outcome – a Pilot Study

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 4230-4230
Author(s):  
Ewa Niedzielska ◽  
Adrian Doroszko ◽  
Alicja Chybicka ◽  
Andrzej Szuba
Keyword(s):  
Lipid Peroxidation ◽  
High Risk ◽  
Risk Stratification ◽  
Endothelial Function ◽  
Risk Group ◽  
High Risk Group ◽  
No Bioavailability ◽  
Anti Inflammatory ◽  
Standard Risk ◽  
Pai 1

Abstract Abstract 4230 Background: Endothelial dysfunction (ED) is characterized by impaired balance between pro- and anti-aggregatory, pro- and anti-inflammatory factors as well as vasodilative and vasoconstrictive action of numerous metabolic and signaling pathways. ED is an important factor worsening the outcome in severe diseases. The aim of this study was to assess if the profile of endothelial function during the treatment of ALL might be associated with the risk stratification and with the outcome. Material and Methods: N=18 children at age of 4–18 years with ALL, treated with the ALLIC- BFM 2002 protocol were investigated. Plasma levels of the NO pathway metabolites (L-Arginine, ADMA – an endogenous competive eNOS inhibitor), markers of endothelial inflammatory and aggregatory function (VCAM-1, ICAM-1, E-selectin, P-selectin and PAI-1), lipid peroxidation (MDA – malonyldialdehyde) were analyzed at baseline, then during the 33rd and 78th day of treatment. Results were compared between three subgroups: standard risk, intermediate risk and high risk. Results: Subjects in the high risk groups were characterized by increased baseline lipid peroxidation, as assessed by the MDA levels in comparison to those in the standard risk group (8.56±2.14U/ml vs. 3.57±0.81U/ml, respectively, p<0.05). In the high risk group low E-selectin levels at baseline (32.1±6.1ng/ml vs. 101.3±11.8ng/ml in the standard risk group, respectively, p<0.05), as well as high NO production at the beginning of the M protocol, assessed by the L-Arg/ADMA ratio (88.6±11.6ng/ml vs. 41.7±6.4ng/ml, respectively, p<0.05) were observed. Moreover, increase in the PAI-1 level during the therapy was associated with smaller risk for poor outcome. Conclusions: Increased lipid peroxidation, low E-selectin at baseline, as well as increased NO bioavailability, decreased PAI-1 levels at the beginning of the M protocol are common feature in children classified to the high risk group. Low NO bioavailability at baseline and high at the beginning of the M protocol as well as decreased anti-inflammatory and antiaggregatory function of endothelium at the beginning of the M protocol are associated with higher risk for poor prognosis. Disclosures: No relevant conflicts of interest to declare.

Operation Everest III: role of plasma volume expansion onV˙o2 max during prolonged high-altitude exposure

2000 ◽  
Vol 89 (1) ◽  
pp. 29-37 ◽  
Author(s):  
Paul Robach ◽  
Michèle Déchaux ◽  
Sébastien Jarrot ◽  
Jenny Vaysse ◽  
Jean-Christophe Schneider ◽  
...  
Keyword(s):  
High Altitude ◽  
Plasma Volume ◽  
Volume Expansion ◽  
Plasma Renin ◽  
Plasma Volume Expansion ◽  
Exercise Induced ◽  
Male Subjects ◽  
Increased Activity ◽  
Volume Decrease

We hypothesize that plasma volume decrease (ΔPV) induced by high-altitude (HA) exposure and intense exercise is involved in the limitation of maximal O2 uptake (V˙o2 max) at HA. Eight male subjects were decompressed for 31 days in a hypobaric chamber to the barometric equivalent of Mt. Everest (8,848 m). Maximal exercise was performed with and without plasma volume expansion (PVX, 219–292 ml) during exercise, at sea level (SL), at HA (370 mmHg, equivalent to 6,000 m after 10–12 days) and after return to SL (RSL, 1–3 days). Plasma volume (PV) was determined at rest at SL, HA, and RSL by Evans blue dilution. PV was decreased by 26% ( P < 0.01) at HA and was 10% higher at RSL than at SL. Exercise-induced ΔPV was reduced both by PVX and HA ( P < 0.05). Compared with SL, V˙o2 max was decreased by 58 and 11% at HA and RSL, respectively.V˙o2 max was enhanced by PVX at HA (+9%, P < 0.05) but not at SL or RSL. The more PV was decreased at HA, the moreV˙o2 max was improved by PVX ( P < 0.05). At exhaustion, plasma renin and aldosterone were not modified at HA compared with SL but were higher at RSL, whereas plasma atrial natriuretic factor was lower at HA. The present results suggest that PV contributes to the limitation ofV˙o2 max during acclimatization to HA. RSL-induced PVX, which may be due to increased activity of the renin-aldosterone system, could also influence the recovery ofV˙o2 max.

Role of the renin–angiotensin–aldosterone system in collecting duct-derived endothelin-1 regulation of blood pressureThis article is one of a selection of papers published in the special issue (part 1 of 2) on Forefronts in Endothelin.

2008 ◽  
Vol 86 (6) ◽  
pp. 329-336 ◽  
Author(s):  
Yuqiang Ge ◽  
Yufeng Huang ◽  
Donald E. Kohan
Keyword(s):  
Blood Pressure ◽  
Collecting Duct ◽  
Plasma Renin ◽  
Similar Degree ◽  
Water Excretion ◽  
Renin Angiotensin ◽  
Endothelin 1 ◽  
And Control ◽  
Renin Content

Renal collecting duct (CD)-specific knockout of endothelin-1 (ET-1) causes hypertension and impaired Na excretion. A previous study noted failure to suppress the renin–angiotensin–aldosterone axis in these knockout (KO) mice, hence the current investigation was undertaken to examine the role of this system in CD ET-1 KO. Renal renin content was similar in kidneys from CD ET-1 KO and control mice during normal Na intake; high-Na intake suppressed renal renin content to a similar degree in KO and control. Plasma renin concentrations paralleled changes in renal renin content. Valsartan, an angiotensin receptor blocker (ARB), abolished the hypertension in CD ET-1 KO mice during normal Na intake. High-Na intake + ARB treatment increased blood pressure in CD ET-1 KO, but not in controls. High-Na intake was associated with reduced Na excretion in CD ET-1 KO animals, but no changes in water excretion or creatinine clearance were noted. Spironolactone, an aldosterone antagonist, also normalized blood pressure in CD ET-1 KO mice during normal Na intake, whereas high-Na intake + spironolactone raised blood pressure only in CD ET-1 KO animals. In summary, hypertension in CD ET-1 KO is partly due to angiotensin II and aldosterone. We speculate that CD-derived ET-1 may regulate, via a novel pathway, renal renin production.

Abstract P314: Effect of Sex on Blood Pressure and Endothelial Dysfunction in the Novel BPH2 Mouse Model of Hypertension

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Sean P Didion
Keyword(s):  
Blood Pressure ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Renin Angiotensin System ◽  
Similar Degree ◽  
The Novel ◽  
Angiotensin System ◽  
Male And Female ◽  
Renin Angiotensin

Very little is known regarding blood pressure and endothelial function between the sexes in the hypertensive BPH2 mouse. Thus, the first goal was determine whether blood pressure and endothelial function are significantly different between male and female BPH2 mice. Information regarding the role of the renin-angiotensin system in the BPH2 mouse is also limited; therefore the second goal was to determine the role of the renin-angiotensin system by treating BPH2 mice with captopril for 4 weeks. Systolic blood pressure (SBP) was significantly elevated (P<0.05) and yet comparable (P>0.05) in male and female BPH2 mice and averaged 140±3 and 136±3 mmHg, respectively, whereas, in control mice SBP averaged 112±4 mmHg. Endothelial responses to acetylcholine in carotid artery were markedly impaired (P<0.05) and to a similar degree in male and female BPH2 mice as compared to controls. Captopril treatment was associated with a significant (P<0.05) reduction in blood pressure of 35±7 and 43±4 mmHg in male and female BPH2 mice, respectively. Captopril also resulted in an improvement of endothelial responses in male and female BPH2 mice. These findings demonstrate that male and female BPH2 mice are equally hypertensive and both sexes are characterized by endothelial dysfunction. In addition, the renin-angiotensin system may contribute to both hypertension and endothelial dysfunction in this model. Taken together, our data define the BPH2 mouse as an important model to compare and contrast the effects of hypertension between the sexes. Supported by NIH HL-107632.

scholarly journals Renin-Angiotensin Activation and Oxidative Stress in Early Heart Failure with Preserved Ejection Fraction

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Smita I. Negi ◽  
Euy-Myoung Jeong ◽  
Irfan Shukrullah ◽  
Emir Veleder ◽  
Dean P. Jones ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Ejection Fraction ◽  
Univariate Analysis ◽  
Renin Angiotensin System ◽  
Preserved Ejection Fraction ◽  
Renin Angiotensin ◽  
Stress Markers ◽  
Ras Activation

Animal models have suggested a role of renin-angiotensin system (RAS) activation and subsequent cardiac oxidation in heart failure with preserved ejection fraction (HFpEF). Nevertheless, RAS blockade has failed to show efficacy in treatment of HFpEF. We evaluated the role of RAS activation and subsequent systemic oxidation in HFpEF. Oxidative stress markers were compared in 50 subjects with and without early HFpEF. Derivatives of reactive oxidative metabolites (DROMs), F2-isoprostanes (IsoPs), and ratios of oxidized to reduced glutathione (EhGSH) and cysteine (EhCyS) were measured. Angiotensin converting enzyme (ACE) levels and activity were measured. On univariate analysis, HFpEF was associated with male sex(p=0.04), higher body mass index (BMI)(p=0.003), less oxidizedEhCyS(p=0.001), lower DROMs(p=0.02), and lower IsoP(p=0.03). Higher BMI (OR: 1.3; 95% CI: 1.1–1.6) and less oxidizedEhCyS (OR: 1.2; 95% CI: 1.1–1.4) maintained associations with HFpEF on multivariate analysis. Though ACE levels were higher in early HFpEF (OR: 1.09; 95% CI: 1.01–1.05), ACE activity was similar to that in controls. HFpEF is not associated with significant systemic RAS activation or oxidative stress. This may explain the failure of RAS inhibitors to alter outcomes in HFpEF.

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.

Sign in / Sign up

Export Citation Format

Share Document