Membrane mineralocorticoid receptors (mMRs) or membrane aldosterone receptors are a group of receptors which bind and are activated by mineralocorticoids such as aldosterone. [1] [2] Unlike the classical nuclear mineralocorticoid receptor (MR), which mediates its effects via genomic mechanisms, mMRs are cell surface receptors which rapidly alter cell signaling via modulation of intracellular signaling cascades. [1] [2] The identities of the mMRs have yet to be fully elucidated, but are thought to include membrane-associated classical MRs [3] [4] as well as yet-to-be-characterized G protein-coupled receptors (GPCRs). [1] [5] Rapid effects of aldosterone were found not be reversed by the MR antagonist spironolactone, indicating additional receptors besides just the classical MR. [6] [7] It has been estimated that as much as 50% of the rapid actions of aldosterone are mediated by mMRs that are not the classical MR, based on findings of insensitivity to classical mR antagonists. [7]
mMRs, along with membrane glucocorticoid receptors (mGRs), have been implicated in the rapid effects of mineralocorticoids in the early central stress response. [2] [3] [4] [8] [9] Aldosterone has been found to have rapid non-genomic effects in the central nervous system, [10] the kidneys, [1] [11] [12] the cardiovascular system, [6] [13] and the colon. [1] [12]
GPER, also known as GPR30, binds and is activated by aldosterone, and may be considered an mMR, although it also binds and is activated by estradiol and is generally described as a membrane estrogen receptor (mER). [7] [14]
Membrane mineralocorticoid receptors (mMRs) or membrane aldosterone receptors are a group of receptors which bind and are activated by mineralocorticoids such as aldosterone. [1] [2] Unlike the classical nuclear mineralocorticoid receptor (MR), which mediates its effects via genomic mechanisms, mMRs are cell surface receptors which rapidly alter cell signaling via modulation of intracellular signaling cascades. [1] [2] The identities of the mMRs have yet to be fully elucidated, but are thought to include membrane-associated classical MRs [3] [4] as well as yet-to-be-characterized G protein-coupled receptors (GPCRs). [1] [5] Rapid effects of aldosterone were found not be reversed by the MR antagonist spironolactone, indicating additional receptors besides just the classical MR. [6] [7] It has been estimated that as much as 50% of the rapid actions of aldosterone are mediated by mMRs that are not the classical MR, based on findings of insensitivity to classical mR antagonists. [7]
mMRs, along with membrane glucocorticoid receptors (mGRs), have been implicated in the rapid effects of mineralocorticoids in the early central stress response. [2] [3] [4] [8] [9] Aldosterone has been found to have rapid non-genomic effects in the central nervous system, [10] the kidneys, [1] [11] [12] the cardiovascular system, [6] [13] and the colon. [1] [12]
GPER, also known as GPR30, binds and is activated by aldosterone, and may be considered an mMR, although it also binds and is activated by estradiol and is generally described as a membrane estrogen receptor (mER). [7] [14]