scholarly journals Resequencing Study Identifies Rare Renin–Angiotensin–Aldosterone System Variants Associated With Blood Pressure Salt-Sensitivity: The GenSalt Study

2017 ◽  
Vol 30 (5) ◽  
pp. 495-501 ◽  
Author(s):  
Tanika N. Kelly ◽  
Changwei Li ◽  
James E. Hixson ◽  
Dongfeng Gu ◽  
Dabeeru C. Rao ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Salt Sensitivity ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin

Abstract P153: Mineralocorticoid Receptor Inhibition Abolishes Sex-specific, Renin Angiotensin Aldosterone System-associated Salt Sensitivity in Female Mice

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Jessica L Faulkner ◽  
Simone Kennard ◽  
Daisy Harwood ◽  
Galina Antonova ◽  
Jane Morwitzer ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Mrna Expression ◽  
Mineralocorticoid Receptor ◽  
Salt Sensitivity ◽  
Plasma Aldosterone ◽  
High Salt ◽  
Male Mice ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Female Mice

Up to half of essential hypertension cases in women are associated with salt sensitive blood pressure (BP) increases, however, the sex-specific mechanisms of salt sensitivity in women are unknown. Our lab has shown that female mice are more sensitive to the hypertensive effects of aldosterone than male mice but it is unknown if aldosterone plays a role in salt sensitivity in female mice. We hypothesized that increasing dietary sodium via a high salt diet would increase blood pressure in female mice which would be abrogated by mineralocorticoid receptor (MR) antagonism. To determine salt sensitivity male and female Balb/C mice were implanted with radiotelemeters for continuous recording of BP. BP was recorded during baseline (7 days) and throughout the administration of a high salt (4% NaCl, HS) diet for 7 days with or without concurrent eplerenone supplementation (daily 200 mg/kg/day). Plasma and kidneys were then harvested. Systolic (SBP) and diastolic (DBP) BP were increased in female mice, but not in males, on HS (7.8±3.3 SBP and 7.8±4.0 DBP Δ change in mmHg in female (P<0.05) vs -3.7±3.1 SBP and 3.1±2.1 DBP in male, respectively, n=7-8). Plasma aldosterone levels were decreased in HS male mice compared to control (224±57 vs 151±19 pg/ml, n=3-5), however, increased modestly in HS females (254±56 vs 394±158 pg/ml, n=3-6). Preliminary data indicated that MR antagonism with eplerenone ablated increases in SBP and DBP in HS female mice, while having no effect on blood pressure in HS males (-22.8 SBP and -23.9 DBP Δ change in mmHg in female vs 1.0 SBP and -1.5 DBP in male, n=2). In addition, and in association with an absence of aldosterone suppression with HS, renal mRNA expression of renin (1.4±0.1-fold, P<0.05, n=5), angiotensinogen (4.4±0.2-fold, P<0.05, n=5), AT1 receptor (52.9±0.9-fold, P<0.05, n=5), MR (1.6±0.2-fold, P<0.05, n=5) and α-ENAC (1.3±0.0-fold, P<0.05, n=5) were increased in HS female mice compared to control females. These data indicate that BP increases in HS female mice are associated with unexpected increases in plasma aldosterone as well as mRNA expression of proteins associated with renin angiotensin aldosterone system activation, which may be novel mechanisms via which females have increased risk for salt sensitive hypertension.

scholarly journals Effect of captopril on blood pressure and renin-angiotensin-aldosterone system in hypertensive patients on hemodialysis.

1982 ◽  
Vol 137 (1) ◽  
pp. 21-31 ◽  
Author(s):  
HIROSHI KANEDA ◽  
TOYOAKI MURATA ◽  
JUN MATSUMOTO ◽  
TAKAKICHI MAETA ◽  
KOZO SHITOMI ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renin Angiotensin Aldosterone System ◽  
Hypertensive Patients ◽  
Renin Angiotensin

scholarly journals Tactics of antihypertensive therapy during COVID-19 pandemic

2021 ◽  
Vol 93 (9) ◽  
pp. 1125-1131
Author(s):  
Valery I. Podzolkov ◽  
Anna Е. Bragina ◽  
Yulia N. Rodionova ◽  
Galina I. Bragina ◽  
Ekaterina E. Bykova
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Diseases ◽  
Arterial Hypertension ◽  
Ace Inhibitor ◽  
Fixed Combination ◽  
Significant Risk ◽  
Effective Control ◽  
Combination Drug ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin

Results of foreign and Russian studies indicate a higher mortality rate of patients with concomitant cardiovascular diseases (CVD) due to the new coronavirus infection COVID-19. It has been proven that arterial hypertension, as one of the significant risk factors for the development of concomitant cardiovascular diseases, is associated with a more severe prognosis of COVID-19. This article presents the results of modern studies and large meta-analyzes of necessity and safety of the use of blockers of the renin-angiotensin-aldosterone system in patients with arterial hypertension and COVID-19. The data of studies show that an angiotensin-converting enzyme inhibitor (ACE inhibitor) and a thiazide-like diuretic is a pathogenetically rational combination. It realizes various ways of lowering blood pressure by reducing the activity of the renin-angiotensin-aldosterone system, which is achieved by using an ACE inhibitor, and natriuresis due to diuretics. As an example, a highly effective fixed combination of drugs is considered, characterized by good tolerance, which consists of an ACE inhibitor lisinopril and a thiazide-like diuretic indapamide of prolonged action. The authors expressed the opinion that the appointment of the fixed combination drug Diroton Plus (Gedeon Richter) will contribute to effective control of blood pressure and organoprotection in conditions of increased thrombogenic and prooxidative potential, characteristic of COVID-19 both in the acute stage and within the post-COVID Syndrome.

scholarly journals Aliskiren, Fosinopril, and Their Outcome on Renin-Angiotensin-Aldosterone System (RAAS) in Rats with Thyroid Dysfunction

2019 ◽  
Vol 2019 ◽  
pp. 1-9
Author(s):  
Susan A. S. Farhadi ◽  
Kawa F. Dizaye
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Positive Control ◽  
Urine Flow ◽  
Angiotensin I ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Group 6 ◽  
Renin Level ◽  
Excretion Rates

Background and Objectives. Thyroid hormones have an important role in the growth and development of various tissues including the kidney, which is the major site of renin release and the consequent angiotensin and aldosterone formation. Therefore any derangement in thyroid function can result in abnormal functioning in the renin-angiotensin-aldosterone system. The current study was undertaken to find the impact of using a direct renin inhibitor (Aliskiren) and an angiotensin-converting enzyme inhibitor (Fosinopril) on the components of the renin-angiotensin-aldosterone system (RAAS) in rats with thyroid dysfunctions. Method. Forty-two male albino rats were divided into three subgroups. First group (6 rats) served as control. Second group (18 rats) served as hyperthyroid group (6 rats positive control, 6 rats given Aliskiren, and 6 rats given Fosinopril). Third group (18 rats) served as hypothyroid group (6 rats positive control, 6 rats given Aliskiren, and 6 rats given Fosinopril). Induction of hyperthyroidism and hypothyroidism was done through daily oral administration of L-Thyroxine and Propylthiouracil, respectively. On day 40 of the study, the rats were sacrificed and blood was collected for estimation of renin, angiotensin I, angiotensin II, aldosterone, TSH, T3, and T4. The collected blood samples were also used for estimation of levels blood urea, serum creatinine, liver enzymes, and serum electrolytes. Blood pressure and urine collection were done on days 1 and 40. The collected urine was used for estimation of urine flow, sodium excretion, and potassium excretion rates. Results. In hypothyroid induced rats, serum renin level dropped as expected, while the use of Aliskiren and Fosinopril on these hypothyroid rats raised renin level due to the feedback mechanism. Both angiotensin I and II were significantly (P <0.05) lower than normal levels in the hypothyroid rats, unlike the level of aldosterone, which was higher than normal level. There was nonsignificant lowering in BP (systolic, diastolic, and mean BP) in the hypothyroid rats. Treatment of these rats with Aliskiren and Fosinopril did not lower the blood pressure more than normal when compared to the hypothyroid group. The hypothyroid rats also showed a decrease in level of serum creatinine. In hyperthyroid rats, there was a rise in levels of serum renin, angiotensin II, and aldosterone; nevertheless, the increase in angiotensin I level was significant. The use of Aliskiren and Fosinopril increased the level of renin nonsignificantly (decreased angiotensin I significantly). Hyperthyroid rats showed a significant increase in systolic, diastolic, and mean blood pressure. Both Aliskiren and Fosinopril increased urine flow, Na+   excretion, and K+ excretion rates. Aliskiren was better at reducing the high blood pressure. Conclusion. Aliskiren and Fosinopril in hyperthyroid rats decreased serum angiotensin I, angiotensin II, and aldosterone. Blockade of renin and inhibition of angiotensin-converting enzyme both resulted in a rebound increase in level of renin in hypothyroid rats. Aliskiren is better at controlling blood pressure in hyperthyroid rats. Urine flow, sodium excretion, and potassium excretion rates were improved by the use of Aliskiren and Fosinopril in hyperthyroid rats.

scholarly journals Hypertension Associated with Fructose and High Salt: Renal and Sympathetic Mechanisms

Nutrients ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 569 ◽  
Author(s):  
Dragana Komnenov ◽  
Peter Levanovich ◽  
Noreen Rossi
Keyword(s):  
Blood Pressure ◽  
Chronic Renal Disease ◽  
Sympathetic Nerves ◽  
Renal Nerve ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Salt Consumption ◽  
High Fructose ◽  
Salt Sensitive Hypertension ◽  
Renal Sympathetic

Hypertension is a leading cause of cardiovascular and chronic renal disease. Despite multiple important strides that have been made in our understanding of the etiology of hypertension, the mechanisms remain complex due to multiple factors, including the environment, heredity and diet. This review focuses on dietary contributions, providing evidence for the involvement of elevated fructose and salt consumption that parallels the increased incidence of hypertension worldwide. High fructose loads potentiate salt reabsorption by the kidney, leading to elevation in blood pressure. Several transporters, such as NHE3 and PAT1 are modulated in this milieu and play a crucial role in salt-sensitivity. High fructose ingestion also modulates the renin-angiotensin-aldosterone system. Recent attention has been shifted towards the contribution of the sympathetic nervous system, as clinical trials demonstrated significant reductions in blood pressure following renal sympathetic nerve ablation. New preclinical data demonstrates the activation of the renal sympathetic nerves in fructose-induced salt-sensitive hypertension, and reductions of blood pressure after renal nerve ablation. This review further demonstrates the interplay between sodium handling by the kidney, the renin-angiotensin-aldosterone system, and activation of the renal sympathetic nerves as important mechanisms in fructose and salt-induced hypertension.

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