Fluid homeostasis is chiefly controlled by the renin-angiotensin-aldosterone system (Figure 1).1 The juxtaglomerular apparatus (JGA) senses low salt load and low blood pressure (BP). In response, renin is released into the vascular compartment where it reacts with angiotensinogen converting it to angiotensin I. Angiotensin I is then converted to angiotensin II via the angiotensin-converting enzyme (ACE). Angiotensin II, a powerful vasoconstrictor, also acts on the adrenal cortex to stimulate the synthesis of aldosterone, which in turn promotes increased uptake of sodium and water and thus the volume expansion necessary to maintain BP. When homeostatic mechanisms fail and the blood volume becomes greater than the limited volume capacity of the vascular compartment, the patient develops high BP.
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