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Although the kidney cannot directly sense blood, long-term regulation of blood pressure predominantly depends upon the kidney.
This primarily occurs through maintenance of the extracellular fluid compartment, the size of which depends on the plasma sodium concentration.
Renin is the first in a series of important chemical messengers that comprise the renin-angiotensin system.
Changes in renin ultimately alter the output of this system, principally the hormones angiotensin II and aldosterone.
Each hormone acts via multiple mechanisms, but both increase the kidney's absorption of sodium chloride, thereby expanding the extracellular fluid compartment and raising blood pressure.
When renin levels are elevated, the concentrations of angiotensin II and aldosterone increase, leading to increased sodium chloride reabsorption, expansion of the extracellular fluid compartment, and an increase in blood pressure.
Conversely, when renin levels are low, angiotensin II and aldosterone levels decrease, contracting the extracellular fluid compartment, and decreasing blood pressure.

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