Eplerenone,
an aldosterone receptor adversary agnate to spironolactone, has been apparent
to aftermath abiding increases in claret renin and serum aldosterone, constant
with inhibition of the abrogating authoritative acknowledgment of aldosterone
on renin secretion. The consistent added claret renin action and aldosterone
circulating levels do not affected the furnishings of eplerenone. Eplerenone
selectively binds to recombinant animal mineralocorticoid receptors about to
its bounden to recombinant animal glucocorticoid, progesterone and androgen
receptors.
Eplerenone
binds to the mineralocorticoid receptor and thereby blocks the bounden of
aldosterone (component of the renin-angiotensin-aldosterone-system, or RAAS).
Aldosterone synthesis, which occurs primarily in the adrenal gland, is
articulate by assorted factors, including angiotensin II and non-RAAS mediators
such as adrenocorticotropic hormone (ACTH) and potassium. Aldosterone binds to
mineralocorticoid receptors in both epithelial (e.g., kidney) and nonepithelial
(e.g., heart, claret vessels, and brain) tissues and increases claret burden
through consecration of sodium reabsorption and possibly added mechanisms.
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