Key result
Low-sodium diet in mast cell-deficient mice unexpectedly induced an exaggerated aldosterone response, leading to severe hyperaldosteronism, increased systolic blood pressure, and marked hypokalemia.
Why the study?
Does a low-sodium diet alter aldosterone secretion in mast cell-deficient mice compared to wild-type mice?
Does a low-sodium diet alter aldosterone secretion in mast cell-deficient mice compared to wild-type mice?
Mast cell-deficient mice represent a novel animal model of primary aldosteronism that is uniquely triggered by sodium restriction.
May implicate adrenal mast cells in aldosterone regulation; leaves open inhibition strategies for primary aldosteronism.
Resident adrenal mast cells have been shown to activate aldosterone secretion in rat and man. Especially, mast cell proliferation has been observed in adrenal tissues from patients with aldosterone-producing adrenocortical adenoma. In the present study, we show that the activity of adrenal mast cells is stimulated by low-sodium diet and correlates with aldosterone synthesis in C57BL/6 and BALB/c mice. We have also investigated the regulation of aldosterone secretion in mast cell–deficient C57BL/6 Kit W-sh/W-sh mice in comparison with wild-type C57BL/6 mice. Kit W-sh/W-sh mice submitted to normal sodium diet had basal plasma aldosterone levels similar to those observed in wild-type animals. Conversely, low-sodium diet unexpectedly induced an exaggerated aldosterone response, which seemed to result from an increase in adrenal renin and angiotensin type 1 receptor expression. Severe hyperaldosteronism was associated with an increase in systolic blood pressure and marked hypokalemia, which favored polyuria. Adrenal renin and angiotensin type 1 receptor overexpression may represent a compensatory mechanism aimed at activating aldosterone production in the absence of mast cells. Finally, C57BL/6 Kit W-sh/W-sh mice represent an unexpected animal model of primary aldosteronism, which has the particularity to be triggered by sodium restriction.
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Boyer et al. (2017) studied Aldosterone secretion regulation. Low-sodium diet vs. Normal sodium diet and wild-type mice was evaluated on Plasma aldosterone levels. Low-sodium diet in mast cell-deficient mice unexpectedly induced an exaggerated aldosterone response, leading to severe hyperaldosteronism, increased systolic blood pressure, and marked hypokalemia.
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