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Figure 1: Renin-Dependent Aldosteronism. The physiologic relationship between the renin-angiotensin system and aldosterone regulation is referred to as “Renin-Dependent Aldosteronism,” also referred to as “Secondary Aldosteronism.” Decreased renal-vascular perfusion resulting in decreased glomerular filtration is sensed by juxtaglomerular cells. The consequent release of renin activates the renin-angiotensin system resulting in the synthesis of angiotensin II (AngII). AngII induces systemic vasoconstriction, increases proximal tubular sodium reabsorption, and stimulates aldosterone secretion. The net effect is increased renal sodium reabsorption and intravascular volume expansion which closes the feedback loop and corrects the initial stimulus to raise renin.

Figure 1: Renin-Dependent Aldosteronism. The physiologic relationship between the renin-angiotensin system and aldosterone regulation is referred to as “Renin-Dependent Aldosteronism,” also referred to as “Secondary Aldosteronism.” Decreased renal-vascular perfusion resulting in decreased glomerular filtration is sensed by juxtaglomerular cells. The consequent release of renin activates the renin-angiotensin system resulting in the synthesis of angiotensin II (AngII). AngII induces systemic vasoconstriction, increases proximal tubular sodium reabsorption, and stimulates aldosterone secretion. The net effect is increased renal sodium reabsorption and intravascular volume expansion which closes the feedback loop and corrects the initial stimulus to raise renin.