• When the glomular cells in the kidney sense that the Na⁺ level in the blood is low, indicating low blood pressure, they release a protease called renin

  Renin, an Aspartate Protease (2ren)

• Renin has only a single substrate, angiotensinogen, from which it clips angiotensin I

• In the liver, angiotensin converting enzyme (ACE), a zinc protease, clips another two residues from angiotensin I, creating angiotensin II
  

  ACE uses Glu384 as the catalytic residue. An activation mechanism involving chloride ions is not understood in any detail. However, ACE is a major target for blood pressure regulating medications such as lisinopril.

  Angiotensin Converting Enzyme (1o8a)	The Catalytic Site
  Angiotensin Converting Enzyme Bound to Liptoprinil (1o86)	The Catalytic Site
  Angiotensin I (1n9u)	Angiotensin II (1n9v)

• In the adrenal cortex, angiotensin II stimulates the production of the steroid hormone aldosterone
  

• Aldosterone causes the kidney to stop secreting Na⁺ into the urine

• Increasing Na⁺ requires retention of fluid, and the blood pressure rises

The cycle also operates in the reverse direction, releasing Na+ when the blood pressure rises.

A disease known as Addison's disease is the total loss of function of the adrenal cortex, resulting in failure to respond to angiotensin, with consequent critically low blood pressure, and other problems related to the concommitant loss of cortisol. President Kennedy had Addison's disease

One case in known in which only the ability to synthesize aldosterone has been lost. The consequence is the same: no blood pressure, the consequence of which is obvious. The case is me.

For either of us, the remedy is the same: