Natriuretic Hormones

Excretion of excess sodium involves not only suppression of salt-retention mechanisms but also activation of sodium-shedding (natriuretic) mechanisms. Two types of hormones are involved: atrial natriuretic peptide (ANP), produced by the cardiac atria when they are overstretched (reduction of ECF volume being an appropriate response to cardiac overload), and active sodium transport inhibitors (ASTIs), probably produced within the brain. These were probably the original molecules associated with the receptors binding cardiac glycoside drugs and are therefore also called 'endogenous digitalis-like inhibitors' (EDLIs);

their exact identity remains uncertain. Atrial natriure-tic peptide has various effects that essentially oppose those of the salt retention induced by aldosterone: it increases sodium excretion, lowers arterial pressure, and promotes movement of ECF towards the interstitial compartment.

Other hormones (e.g., sex steroids, parathyroid hormone, calcitonin, thyroid hormone, prolactin) affect renal sodium retention or loss but are not thought to regulate it.

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