Primary aldosteronism (PA) is a type of secondary hypertension that is caused by aldosterone overproduction and oversecretion from the adrenal glands. Aldosterone-producing adenoma (APA) of the unilateral adrenal cortex accounts for 80–90% of PA cases; the remaining 10–20% are bilateral idiopathic hyperaldosteronism (IHA).
PA is more likely to be complicated by myocardial infarction and stroke compared with essential hypertension (EHT). This finding may be due to worse endothelial function that is caused by higher circulating levels of aldosterone in PA compared with that in EHT.
A previous study showed that flow-mediated dilation (FMD) was significantly lower in patients with APA than in those with IHA and EHT [1]. In the present study, the authors demonstrated that microvascular, but not macrovascular, endothelial function was impaired in patients with IHA compared to those with EHT, although FMD was similar between IHA and EHT patients [2].
Microvascular endothelial function was evaluated using the log-transformed reactive hyperemic index (log RHI) as measured by RH-peripheral arterial tonometry (RH-PAT) [2]. FMD and log RHI reflect macrovascular and microvascular endothelial functions, respectively [3, 4].
Aldosterone increases inflammation and fibrosis in the vasculature, resulting in endothelial dysfunction [5,6,7,8]. Moderately elevated plasma aldosterone concentration (PAC) in IHA impairs microvascular endothelial function, whereas the greatly elevated PAC in APA impairs both microvascular and macrovascular endothelial functions.
Surgical resection of APA improved FMD in patients with APA [1]. However, it remains unclear whether mineralocorticoid receptor antagonists, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, renin inhibitors, beta-blockers, and some calcium channel blockers can improve the log RHI in patients with IHA (Table 1). Further studies are needed to elucidate this issue.
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Kato, T., Node, K. Microvascular and macrovascular endothelial function in two different types of primary aldosteronism. Hypertens Res 42, 739–740 (2019). https://doi.org/10.1038/s41440-018-0153-y
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DOI: https://doi.org/10.1038/s41440-018-0153-y
