scholarly journals Angiotensin II and the Natriuretic and Blood Pressure Response to Mental Stress in African Americans

2018 ◽  
Vol 28 (4) ◽  
pp. 511-516 ◽  
Author(s):  
Gregory A. Harshfield ◽  
Coral D. Hanevold ◽  
Allison Jasti ◽  
Santu Ghosh ◽  
Jennifer Pollock ◽  
...  
Keyword(s):  
Blood Pressure ◽  
African Americans ◽  
Mental Stress ◽  
Blood Pressure Response ◽  
Urinary Sodium Excretion ◽  
Ang Ii ◽  
Placebo Condition ◽  
Double Blind ◽  
Response To Stress ◽  
Study Participants

Objectives: To test the hypothesis that An­giotensin II (Ang II) is a contributing factor to the response pattern in African Americans (AAs) who retain rather than excrete sodium during mental stress.Design/Study Participants: Double-blind, randomized, cross-over trial of 87 healthy AAs aged 18 to 50 years.Interventions: The study participants received either a placebo or irbesartan, (150 mg PO), an Ang II receptor antagonist, for seven days prior to stress testing. Urinary sodium excretion (UNaV) and systolic blood pressure (SBP) were collected prior to and throughout a mental stress protocol (rest and stress period).Setting: A southeastern university.Main Outcome Measures: Ang II, SBP, and sodium retention.Results: During the placebo condition, 62 participants showed the expected increase in UNaV (excreters) while 25 participants reduced UNaV during stress (retainers). Irbesartan retainers demonstrated a reversal in the direction of their natriuretic response, now increasing UNaV in response to stress (Δ UNaV of -.094 mmol/min with placebo vs .052 mmol/min on irbesartan; P<.001). In excreters, irbesartan reduced SBP levels during both rest (-2.36 mm Hg; P=.03) and stress (-4.59;P<.0001), and an even more pronounced reduction in SBP was dem­onstrated by retainers on treatment during both rest (-4.29 mm Hg; P=.03) and stress (-6.12; P<.001).Conclusions: Ang II contributes to sodium retention in retainers. Furthermore, our findings indicate that suppression of Ang II has a beneficial effect on SBP during rest and stress in this population.Ethn Dis. 2018;28(4):511-516; doi:10.18865/ed.28.4.511.

Abstract 634: Suppression of Ang II Inhibits Sodium Retention During Mental Stress

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Gregory A Harshfield ◽  
Coral Hanevold ◽  
Luis Ortiz ◽  
Obioma I Nwobi ◽  
Maribeth Johnson ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Video Game ◽  
Mental Stress ◽  
Sodium Intake ◽  
Controlled Trial ◽  
Ang Ii ◽  
Angiotensin Receptor ◽  
Placebo Condition ◽  
Double Blind ◽  
Sodium Load

Background: We hypothesized that stress-induced increases in Ang-II would increase the retained sodium load over the course of a day in a significant percentage of African-Americans (AAs). Methods: We tested this hypothesis with a double blind placebo-controlled trial which examined the effect of an angiotensin receptor antagonist blocker (irbesartan) on the pressure natriuresis response to one hour of mental stress induced by a competitive video game task in 93 healthy, normotensive AAs with a mean age of 26 years. The 3-hour protocol consisted of a 1-hour stress period preceded and followed by a 1-hour rest period. Blood and urine were collected hourly and blood pressure at 15 minute intervals. The subjects were divided into those who increased (excreters, upper panel) or decreased (retainers, lower panel) U Na V with stress in the placebo condition. Results: The ARB increased the change in U Na V during stress by 10.2 mEq, or approximately 235 mgs in Retainers but had no effect in Excreters. The ARB also had a beneficial effect on the blood pressure levels in Retainers but not Excreters, lowering levels throughout the protocol in this group. Conclusions: Assuming 4 episodes of stress during a day, the additional sodium load induced by Ang II would be approximately 1,000 mgs, which would increase the average intake by an estimated one third. From a prevention perspective, these individuals would need to reduce their sodium intake by a third to compensate for the amount of sodium reabsorbed during episodes of mental stress throughout the day. Figure. Effect of angiotensin receptor blocker on sodium excretion (UnaV) in response to stress in AA excreters vs. retainers.

scholarly journals State Anxiety Is Associated with Cardiovascular Reactivity in Young, Healthy African Americans

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Mildred A. Pointer ◽  
Sadiqa Yancey ◽  
Ranim Abou-Chacra ◽  
Patricia Petrusi ◽  
Sandra J. Waters ◽  
...  
Keyword(s):  
Blood Pressure ◽  
African Americans ◽  
Cardiovascular Reactivity ◽  
Trait Anxiety ◽  
State Anxiety ◽  
Blood Pressure Response ◽  
Cold Pressor ◽  
Pressure Response ◽  
Anxiety State ◽  
Stress Tests

Although several studies have shown that enhanced cardiovascular reactivity can predict hypertension development in African Americans, these findings have not been consistent among all studies examining reactivity and hypertension susceptibility. This inconsistency may be explained by the influence of anxiety (state and trait) on the blood pressure response to stress. Therefore, this study sought to determine whether anxiety is associated with blood pressure response to cold pressor (CP) and anger recall (AR) stress tests in young healthy African Americans. Modeling using state and trait anxiety revealed that state anxiety predicts systolic (SBP) and diastolic blood pressure DBP response to CP and AR (P≤0.02). Interestingly, state anxiety predicted heart rate changes only to CP (P<0.01;P=0.3for AR). Although trait anxiety was associated with SBP response to AR and not CP, it was not a significant predictor of reactivity in our models. We conclude that anxiety levels may contribute to the variable blood pressure response to acute stressors and, therefore, should be assessed when performing cardiovascular reactivity measures.

Abstract 17321: Race Differences in Hemodynamic Responses to Acute Mental Stress and the Role of Depressive Symptoms

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Kobina A Wilmot ◽  
Ibhar Al Mheid ◽  
Ronnie Ramadan ◽  
Pratik M Pimple ◽  
Amit J Shah ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Depressive Symptoms ◽  
African Americans ◽  
Mental Stress ◽  
Rate Pressure Product ◽  
Hemodynamic Responses ◽  
Explanatory Role ◽  
The Difference ◽  
Hemodynamic Reactivity ◽  
Different Response

Introduction: Increased hemodynamic responses to psychological stress have been associated with adverse CAD events. African Americans (AA) have worse CAD outcomes than other groups. Heightened hemodynamic responses to stress may play a role. Our hypothesis was that AA would have higher hemodynamic reactivity to a standardized mental stress compared to Non-African Americans (NAA). Methods: We evaluated 574 patients (163 AA) with CAD, who underwent a standardized mental stress challenge. Hemodynamics were obtained at rest, during stress (speaking task), and during recovery. The rate-pressure product (RPP) was calculated as systolic blood pressure (SBP) x heart rate (HR). Hemodynamic reactivity was evaluated as the difference in RPP at rest and during stress. Depressive symptoms were measured with the Beck Depression Inventory-II (BDI). Results: As compared to NAA, AA patients were younger, had lower education and income, and higher prevalence of diabetes, obesity, hypertension, smoking, and depressive symptoms (BDI mean scores 9.8 vs. 7.6, p= 0.003). AA patients had higher blood pressure during all three periods (Table). However, hemodynamic reactivity with stress was significantly lower in AA than NAA (RPP reactivity 3114 vs 3620, p= 0.02). Adjusting for baseline RPP, age, gender and smoking did not substantially alter the association. However, after adjusting for depressive symptoms, the association was attenuated by 23% (p=0.16). BMI, diabetes and beta-blocker use had minimal additional explanatory role. In the final model, baseline RPP, depressive symptoms and BMI were significantly associated with a lower RPP reactivity (p<0.01). Conclusion: AA patients with CAD, compared with NAA, have elevated blood pressure throughout mental stress, but tend to have blunted hemodynamic reactivity to stress. Depressive symptoms, which are more elevated among AA, play a role in this different response to stress and may be implicated in the higher CAD risk of this group.

Comparison of fast and slow pressor effects of angiotensin II in the conscious rat

1981 ◽  
Vol 241 (3) ◽  
pp. H381-H388 ◽  
Author(s):  
A. J. Brown ◽  
J. Casals-Stenzel ◽  
S. Gofford ◽  
A. F. Lever ◽  
J. J. Morton
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Pressor Response ◽  
Control Period ◽  
Urinary Sodium Excretion ◽  
Sodium Balance ◽  
Pressor Effect ◽  
Ang Ii ◽  
Conscious Rat ◽  
Female Wistar Rats

Female Wistar rats were infused intravenously with 5% dextrose for 3 days, then with angiotensin II (ANG II) in 5% dextrose at 20 ng . kg-1 . min-1 for 7 days, and finally with dextrose for 2.5 days. ANG II raised mean arterial pressure (MAP) gradually; by the 7th day it was 49.7 mmHg higher than during the dextrose control period in the same rats. Control rats were infused with dextrose for 12.5 days; MAP did not change. Plasma ANG II concentration was measured during infusion. In hypertensive rats on the 7th day of ANG II infusion, it was six times higher than in control rats infused with dextrose. Changes of blood pressure and plasma ANG II concentration were compared in further rats infused with much larger doses of ANG II. Rats receiving 270 ng . kg-1 . min-1 for 1 h had an almost maximal direct pressor response, MAP rising 45.3 mmHg and plasma ANG II rising 32-fold compared with controls. Thus, infusion of ANG II at low dose without direct pressor effect gradually raises blood pressure to a level similar to the maximum direct pressor effect produced by larger doses of ANG II. Sodium balance and food and water intakes were also measured and did not change during prolonged infusion of ANG II at 20 ng . kg-1 . min-1. Thus, the slow pressure effect of ANG II develops at a lower and more nearly physiological plasma concentration of the peptide than do the direct pressor effect and the effects on drinking, eating, and urinary sodium excretion.

scholarly journals Salivary uric acid: Associations with resting and reactive blood pressure response to social evaluative stress in healthy African Americans

2019 ◽  
Vol 101 ◽  
pp. 19-26 ◽  
Author(s):  
Jacqueline Woerner ◽  
Todd Lucas ◽  
Jennifer Pierce ◽  
Jenna L. Riis ◽  
Douglas A. Granger
Keyword(s):  
Blood Pressure ◽  
Uric Acid ◽  
African Americans ◽  
Blood Pressure Response ◽  
Pressure Response

ACE inhibition and ANG II receptor blockade improve glomerular size-selectivity in IgA nephropathy

1999 ◽  
Vol 276 (3) ◽  
pp. F457-F466 ◽  
Author(s):  
Andrea Remuzzi ◽  
Norberto Perico ◽  
Fabio Sangalli ◽  
Giovanni Vendramin ◽  
Monica Moriggi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Iga Nephropathy ◽  
Ace Inhibitors ◽  
Ace Inhibition ◽  
Maximum Effect ◽  
Double Blind Study ◽  
Ang Ii ◽  
Size Selectivity ◽  
Double Blind ◽  
Glomerular Size

Protein trafficking across the glomerular capillary has a pathogenic role in subsequent renal damage. Despite evidence that angiotensin-converting enzyme (ACE) inhibitors improve glomerular size-selectivity, whether this effect is solely due to ANG II blocking or if other mediators also play a contributory role is not clear yet. We studied 20 proteinuric patients with IgA nephropathy, who received either enalapril (20 mg/day) or the ANG II receptor blocker irbesartan (100 mg/day) for 28 days in a randomized double-blind study. Measurements of blood pressure, renal hemodynamics, and fractional clearance of neutral dextran of graded sizes were performed before and after 28 days of treatment. Both enalapril and irbesartan significantly reduced blood pressure over baseline. This reduction reached the maximum effect 4–6 h after drug administration but did not last for the entire 24-h period. Despite transient antihypertensive effect, proteinuria was effectively reduced by both treatments to comparable extents. Neither enalapril nor irbesartan modified the sieving coefficients of small dextran molecules, but both effectively reduced transglomerular passage of large test macromolecules. Theoretical analysis of sieving coefficients showed that neither drug affected significantly the mean pore radius or the spread of the pore-size distribution, but both importantly and comparably reduced the importance of a nonselective shunt pathway. These data suggest that antagonism of ANG II is the key mechanism by which ACE inhibitors exert their beneficial effect on glomerular size-selective function and consequently on glomerular filtration and urinary output of plasma proteins.

scholarly journals Genetic deletion of AT1a receptors attenuates intracellular accumulation of ANG II in the kidney of AT1a receptor-deficient mice

2007 ◽  
Vol 293 (2) ◽  
pp. F586-F593 ◽  
Author(s):  
Xiao C. Li ◽  
L. Gabriel Navar ◽  
Yuan Shao ◽  
Jia L. Zhuo
Keyword(s):  
Blood Pressure ◽  
Sodium Excretion ◽  
Rat Kidney ◽  
Systolic Pressure ◽  
Weight Ratio ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Ang Ii ◽  
Wild Type ◽  
Deficient Mice

We and others have previously shown that high levels of ANG II are accumulated in the rat kidney via a type 1 (AT1) receptor-mediated mechanism, but it is not known which AT1 receptor is involved in this process in rodents. We tested the hypothesis that AT1a receptor-deficient mice (Agtr1a−/−) are unable to accumulate ANG II intracellularly in the kidney because of the absence of AT1a receptor-mediated endocytosis. Adult male wild-type (Agtr1a+/+), heterozygous (Agtr1a+/−), and Agtr1a−/− were treated with vehicle, ANG II (40 ng/min ip via osmotic minipump), or ANG II plus the AT1 antagonist losartan (10 mg·kg−1·day−1 po) for 2 wk. In wild-type mice, ANG II induced hypertension (168 ± 4 vs. 113 ± 3 mmHg, P < 0.001), increased kidney-to-body weight ratio ( P < 0.01), caused pressure natriuresis ( P < 0.05), and elevated plasma and whole kidney ANG II levels ( P < 0.001). Concurrent administration of ANG II with losartan attenuated these responses to ANG II. In contrast, Agtr1a−/− mice had lower basal systolic pressures ( P < 0.001), smaller kidneys with much fewer AT1b receptors ( P < 0.001), higher basal 24-h urinary sodium excretion ( P < 0.01), as well as basal plasma and whole kidney ANG II levels ( P < 0.01). However, intracellular ANG II levels in the kidney were lower in Agtr1a−/− mice. In Agtr1a−/− mice, ANG II slightly increased systolic pressure ( P < 0.05) but had no effect on the kidney weight, urinary sodium excretion, and whole kidney ANG II levels. Losartan restored systolic pressure to basal levels and decreased whole kidney ANG II levels by ∼20% ( P < 0.05). These results demonstrate a predominant role of AT1a receptors in blood pressure regulation and in the renal responses to long-term ANG II administration, that AT1b receptors may play a limited role in blood pressure control and mediating intrarenal ANG II accumulation in the absence of AT1a receptors.

scholarly journals Blood Pressure Response to Zofenopril or Irbesartan Each Combined with Hydrochlorothiazide in High-Risk Hypertensives Uncontrolled by Monotherapy: A Randomized, Double-Blind, Controlled, Parallel Group, Noninferiority Trial

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Ettore Malacco ◽  
Stefano Omboni ◽  
Gianfranco Parati
Keyword(s):  
Blood Pressure ◽  
Renal Damage ◽  
Blood Pressure Response ◽  
Target Organ Damage ◽  
Organ Damage ◽  
Target Organ ◽  
Double Blind ◽  
Treatment Groups ◽  
Parallel Group ◽  
Plaque Regression

In this randomized, double-blind, controlled, parallel group study (ZENITH), 434 essential hypertensives with additional cardiovascular risk factors, uncontrolled by a previous monotherapy, were treated for 18 weeks with zofenopril 30 or 60 mg plus hydrochlorothiazide (HCTZ) 12.5 mg or irbesartan 150 or 300 mg plus HCTZ. Rate of office blood pressure (BP) response (zofenopril: 68% versus irbesartan: 70%;p=0.778) and 24-hour BP response (zofenopril: 85% versus irbesartan: 84%;p=0.781) was similar between the two treatment groups. Cardiac and renal damage was equally reduced by both treatments, whereas the rate of carotid plaque regression was significantly larger with zofenopril. In conclusion, uncontrolled monotherapy treated hypertensives effectively respond to a combination of zofenopril or irbesartan plus a thiazide diuretic, in terms of either BP response or target organ damage progression.

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