Angiotensin converting enzyme, or

ACE, as it is known, is secreted by our

lungs in response to low blood pressure
or decreased blood volume
(hypovolemia), and it converts
angiotensin I into a more powerful
vasoconstrictor, angiotensin II.

Angiotensin II acts on the renal

vasculature to constrict efferent
arteriole, in order to maintain
glomerular filtration rate (GFR). This in
turn, also leads to increase in the blood
pressure, as concomitantly secreted
aldosterone helps in fluid and salt
conservation by the kidneys.

In diseases like hypertension and

diabetes mellitus, nephropathic and vascular injuries result in increased amount of protein being filtered by the glomerulus, which
is subsequently lost in the urine.

ACE inhibitors, such as enalapril, captopril, etc., stop this

entire cascade from forming, by inhibiting the ACE enzyme.
Hence, a reduction in the GFR will also reduce the amount
of protein being filtered by the nephrons, thus, serving the
dual function of reducing the
hypertension/hypervolemia/hypernatraemia and reducing
the proteinuria.

One has to be careful in prescribing these medications to

those patients who have preexisting renal artery stenosis,
especially when present bilaterally, because an ACE
mediated vasoconstriction of the efferent arteriole is what is
keeping the flitration pressure from dropping, which will
reduce GFR, and with that, cause renal failure.

Reduced perfusion pressure with an angiotensin-

converting enzyme
inhibitor (ACE-I) or an angiotensin receptor blocker
(ARB). Loss of angiotensin II action reduces efferent
resistance; this causes the glomerular
capillary pressure to drop below normal values and
the GFR to decrease. (From JG Abuelo: N Engl J Med
357:797-805, 2007; with permission.)