2013
DOI: 10.1093/ajh/hpt091
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Bimodal Aldosterone Distribution in Low-Renin Hypertension

Abstract: In this community-based sample of white subjects, those with low-renin hypertension had a bimodal adjusted aldosterone distribution. Subjects with normal-renin hypertension and subjects with normal blood pressure had unimodal adjusted aldosterone distributions. These findings suggest 2 pathophysiological variants of LRH, one that is aldosterone-dependent and one that is non-aldosterone-dependent.

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Cited by 25 publications
(19 citation statements)
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“…More importantly, the aforementioned limitation does not degrade the validity of our observational findings which are supported by physiologic principles: 1) the decoupling of elevated aldosterone levels and suppression of renin that associated with the highest risk for incident hypertension (Figure 1A) cannot be explained by dietary sodium balance, rather can only be explained as an autonomous or renin-independent aldosteronism; 2) conversely, renin-dependent aldosterone secretion (Figure 1C) cannot be ascribed to autonomous aldosterone secretion since renin was not suppressed, and was therefore presumptively physiologic. Further, the suppressed renin phenotype (PRA ≤ 0.50 μg/L/h) was probably comprised of a combination of: participants with “normal” physiology who displayed an appropriately suppressed renin and aldosterone while on a relatively high sodium intake; participants who had autonomous aldosteronism despite renin suppression and high sodium intake (renin-independent aldosterone secretion); and possibly also participants with suppressed renin and aldosterone due to non-aldosterone MR ligands that were not directly assessed in the current study(42, 43). Thus, this heterogeneous mixture of normal (physiologic) and abnormal (pathophysiologic) phenotypes when PRA was ≤ 0.50 μg/L/h should have favored the null hypothesis by decreasing the enrichment and detectability of autonomous aldosteronism.…”
Section: Discussionmentioning
confidence: 99%
“…More importantly, the aforementioned limitation does not degrade the validity of our observational findings which are supported by physiologic principles: 1) the decoupling of elevated aldosterone levels and suppression of renin that associated with the highest risk for incident hypertension (Figure 1A) cannot be explained by dietary sodium balance, rather can only be explained as an autonomous or renin-independent aldosteronism; 2) conversely, renin-dependent aldosterone secretion (Figure 1C) cannot be ascribed to autonomous aldosterone secretion since renin was not suppressed, and was therefore presumptively physiologic. Further, the suppressed renin phenotype (PRA ≤ 0.50 μg/L/h) was probably comprised of a combination of: participants with “normal” physiology who displayed an appropriately suppressed renin and aldosterone while on a relatively high sodium intake; participants who had autonomous aldosteronism despite renin suppression and high sodium intake (renin-independent aldosterone secretion); and possibly also participants with suppressed renin and aldosterone due to non-aldosterone MR ligands that were not directly assessed in the current study(42, 43). Thus, this heterogeneous mixture of normal (physiologic) and abnormal (pathophysiologic) phenotypes when PRA was ≤ 0.50 μg/L/h should have favored the null hypothesis by decreasing the enrichment and detectability of autonomous aldosteronism.…”
Section: Discussionmentioning
confidence: 99%
“…PRA was not significantly different in Greyhounds, suggesting that the higher SP in Greyhounds may be most consistent with normal renin hypertension. In people with normal‐renin essential hypertension, plasma aldosterone concentrations tend to have a unimodal distribution that parallels PRA and PRA falls within the normal reference interval . The Greyhounds with normal PRA and low aldosterones do not completely fit with this condition.…”
Section: Discussionmentioning
confidence: 99%
“…In people with normal-renin essential hypertension, plasma aldosterone concentrations tend to have a unimodal distribution that parallels PRA and PRA falls within the normal reference interval. 32,33 The Greyhounds with normal PRA and low aldosterones do not completely fit with this condition. Alternatively, a variety of albuminuric conditions have been recognized in people to be associated with low aldosterone, variable ANP, salt sensitivity, and hypertension which appear to be related to alterations in renal tubular sodium channel activity.…”
Section: Discussionmentioning
confidence: 99%
“…терону, які беруть участь у блокаді ендотеліальної синтази оксиду азоту (NO) і знижують спорідненість ендотеліоцитів до NO [12][13][14].…”
Section: в п о м о щ ь п р а к т и ч е с к о м у в р а ч уunclassified
“…Незважаючи на відомий факт про те, що активація РААС призводить до прогресування судинного ремоделювання, недостатньо вивченим залишається оцінювання її впливу при різній активності компонентів РААС, що відрізняє низькоренінову і високоренінову АГ (НРАГ і ВРАГ відповідно) [10][11][12][13][14].…”
unclassified