The resulting rise in blood pressure closes the normal feedback loop by inhibiting renin release, decreasing RAAS activation, and reducing aldosterone production.[2e],[6d]
1RAAS Activation
2Increased BP
3Feedback loop
Decreased renal perfusion and salt concentration leads to renin release and RAAS pathway activation. Angiotensin II stimulates aldosterone production in the adrenal glands, mediated by aldosterone synthase.[1c],[2c],[5b],[6b]
Aldosterone binds to mineralocorticoid receptors in the kidneys, increasing reabsorption of urinary sodium and raising intravascular volume.[1d],[2d],[5c],[6c]
The resulting rise in blood pressure closes the normal feedback loop by inhibiting renin release, decreasing RAAS activation, and reducing aldosterone production.[2e],[6d]
Aldosterone binds to mineralocorticoid receptors in the kidneys, increasing reabsorption of urinary sodium and raising intravascular volume.[1d],[2d],[5c],[6c]
The resulting rise in blood pressure closes the normal feedback loop by inhibiting renin release, decreasing RAAS activation, and reducing aldosterone production.[2e],[6d]