Aldosterone-to-renin ratio and blood pressure in young adults from the general population

Aeschbacher, Stefanie; Mongiat, Michel; Bernasconi, Raffaele; Blum, Steffen; Meyre, Pascal; Krisai, Philipp; Ceylan, Selinda; Risch, Martin; Risch, Lorenz; Conen, David

doi:10.1016/j.ahj.2019.11.022

Cited by 4 publications

(4 citation statements)

References 35 publications

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“…Our mice experienced an insignificant decrease in plasma aldosterone and a significant decline in ARR. ARR is strongly associated with BP [ 38 ], indicating a propensity in mice with a Prdm16 deletion for hypotension. In addition, we noted less sodium reabsorption in mice with cardiac loss of Prdm16 , also supporting the lowered BP.…”

Section: Discussionmentioning

confidence: 99%

A cardiac-null mutation of Prdm16 causes hypotension in mice with cardiac hypertrophy via increased nitric oxide synthase 1

Kang

Ha²,

Jung³

et al. 2022

PLoS ONE

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Hypertension or hypotension prevails as a comorbidity in patients with heart failure (HF). Although blood pressure (BP) is an important factor in managing the mortality of HF, the molecular mechanisms of changes in BP have not been clearly understood in cases of HF. We and others have demonstrated that a loss in PRDM16 causes hypertrophic cardiomyopathy, leading to HF. We aimed to determine whether BP is altered in mice that experience cardiac loss of Prdm16 and identify the underlying mechanism of BP-associated changes. BP decreased significantly only in female mice with a cardiac-null mutation of Prdm16 compared with controls, by an invasive protocol under anesthesia and by telemetric method during conscious, unrestrained status. Mice with a cardiac loss of Prdm16 had higher heart-to-body weight ratios and upregulated atrial natriuretic peptide, suggesting cardiac hypertrophy. Plasma aldosterone-to-renin activity ratios and plasma sodium levels decreased in Prdm16-deficient mice versus control. By RNA-seq and in subsequent functional analyses, Prdm16-null hearts were enriched in factors that regulate BP, including Adra1a, Nos1, Nppa, and Nppb. The inhibition of nitric oxide synthase 1 (NOS1) reverted the decrease in BP in cardiac-specific Prdm16 knockout mice. Mice with cardiac deficiency of Prdm16 present with hypotension and cardiac hypertrophy. Further, our findings suggest that the increased expression of NOS1 causes hypotension in mice with a cardiac-null mutation of Prdm16. These results provide novel insights into the molecular mechanisms of hypotension in subjects with HF and contribute to our understanding of how hypotension develops in patients with HF.

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Section: Discussionmentioning

confidence: 99%

A cardiac-null mutation of Prdm16 causes hypotension in mice with cardiac hypertrophy via increased nitric oxide synthase 1

Kang

Ha²,

Jung³

et al. 2022

PLoS ONE

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“…14 Another study of 1353 population-based adults with a mean age of 36 years similarly found a positive relationship between the ARR and BP. 15 The relationship between aldosterone and BP in younger populations is less clear. In a study of normotensive men with a mean age of 25 years and a positive family history of hypertension, participants had less than expected suppression of aldosterone in response to saline infusion, suggesting dysregulated aldosterone production.…”

Section: See Editorial Pp 397-399mentioning

confidence: 99%

Relationship Between the Aldosterone-to-Renin Ratio and Blood Pressure in Young Adults: A Longitudinal Study

et al. 2021

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Hypertension tracks throughout childhood into adulthood. Elevated aldosterone in the setting of low renin predicts incident hypertension in normotensive adults, but the relationship is unclear in adolescents and young adults. To explore this relationship, we analyzed data from the offsprings (Gen2) of women enrolled during pregnancy into the Raine Study (population-based birth cohort), who had blood pressure (BP) measurements and blood samples at age 17 years (N=871) and age 27 years (N=758). At 17 years, females had similar median aldosterone levels (349 versus 346 pmol/L) but significantly lower direct renin concentration (20.6 versus 25.7 mU/L) and thus a higher aldosterone-to-renin ratio (ARR; 18.3 versus 13.5) compared with males. However, females had lower systolic BP (109 versus 118 mm Hg) versus males. A significant association between ARR and systolic BP was detected in 17 years males when adjusted for alcohol consumption, physical activity, and body mass index. This was true whether the ARR was expressed as a continuous variable (β-coefficient 0.1, P =0.009) or categorical variable (highest versus lowest quartile, β-coefficient 3.15, P =0.003). No such correlation was observed in females at 17 years. However, the ARR at 17 years was significantly associated with both systolic (β-coefficient 0.15, P =0.009) and diastolic BP (β-coefficient 0.14, P =0.003) at 27 years among females, but not males. The sexually dimorphic relationship between the ARR and BP in 17 and 27 years participants suggests that the ARR, calculated from the plasma aldosterone concentration and direct renin concentration, could be a useful tool for BP prediction and assessment in young people, but require sex-specific interpretation.

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“…In the authors' opinion, the latter finding could be a consequence of the putative insulin-mediated reninindependent sodium reabsorption, volume expansion, and renin inhibition in obesity. In young, healthy 1353 adults aged 25-41 years, blood pressure was directly related to aldosterone, the aldosterone-renin ratio, and inversely to renin concentration [15]. The authors hypothesized that blood pressure rise could be driven in this cohort by a renin-independent aldosterone mechanism and some of the studied patients could have unrecognized primary aldosteronism.…”

Section: Discussionmentioning

confidence: 99%

“…Finally, 51 children with untreated primary hypertension were enrolled in the study, and the control group consisted of 45 age-and sex-matched healthy children. The sample size was estimated based on the available literature on renin with a statistical power of 0.8, p = 0.05, and an effect size of 0.55 should be 45 [10][11][12][13][14][15].…”

Section: Study Groupmentioning

confidence: 99%

Evaluation of Active Renin Concentration in A Cohort of Adolescents with Primary Hypertension

Deja

Skrzypczyk

Nowak

et al. 2022

IJERPH

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Our study aimed to assess active renin concentration in children with primary hypertension. Thus, we evaluated active renin concentration, clinical parameters, office and ambulatory blood pressure, and biochemical parameters in 51 untreated adolescents with primary hypertension (median: 14.4 [interquartile range—IQR: 13.8–16.8] years) and 45 healthy adolescents. Active renin concentration did not differ between patients with hypertension and healthy children (median: 28.5 [IQR: 21.9–45.2] vs. 24.9 [IQR: 16.8–34.3] [pg/mL], p = 0.055). In the whole group of 96 children, active renin concentration correlated positively with serum potassium and office and ambulatory systolic and diastolic blood pressures. Among children with hypertension, patients with isolated systolic hypertension had lower renin concentration than patients with systolic-diastolic hypertension (26.2 [IQR: 18.6–34.2] vs. 37.8 [IQR: 27.0–49.6] [pg/mL], p = 0.014). The active renin concentration did not differ between patients with isolated systolic hypertension and healthy children. In multivariate analysis, diastolic blood pressure Z-score (beta = 0.238, 95 confidence interval [0.018–0.458], p = 0.035) was the only predictor of active renin concentration in the studied children. We concluded that active renin concentration is positively associated with blood pressure and potassium in children, and diastolic blood pressure was the strongest predictor of renin level. Patients with isolated systolic hypertension may differ from patients with systolic-diastolic hypertension in less severe activation of the renin-angiotensin-aldosterone system.

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Aldosterone-to-renin ratio and blood pressure in young adults from the general population

Cited by 4 publications

References 35 publications

A cardiac-null mutation of Prdm16 causes hypotension in mice with cardiac hypertrophy via increased nitric oxide synthase 1

A cardiac-null mutation of Prdm16 causes hypotension in mice with cardiac hypertrophy via increased nitric oxide synthase 1

Relationship Between the Aldosterone-to-Renin Ratio and Blood Pressure in Young Adults: A Longitudinal Study

Evaluation of Active Renin Concentration in A Cohort of Adolescents with Primary Hypertension

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