ANP is secreted by atrial cells in response to fluid overload in order to decrease fluid levels. It does this by inhibiting sodium reuptake in the principal cells of the collecting duct.
ANPs binds to prinicpal cells and activates guanylyl cyclase, produceing cGMP that inhibits Na channels.
ANP also inhibits aldosterone release and renin production, increasing GFR by dilating afferent arterioles.
The net effect is to increase sodium excretion and induce fluid loss.
Patients with Heart Failure show resistance to the diuretic effects of ANP, possibly due to diminished sodium delivery, due to anti-natriuretic / vasoconstrictor hormones such as Ang II.
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