the antihypertensive prototype angiotensin converting enzyme inhibitor
What is the deal with ACE Inhibitors?
Angiotensin converting enzyme (ACE) converts angiotensin I into angiotensin II. The idea here is that there is a cascade of activity that follows the conversion of angiotensin I into angiotensin II is stopped when you add a drug such as captopril into the system.
The renin-angiotensin-aldosterone (RAA) is one of the body’s ways of altering circulating fluid volume and peripheral resistance.
Try and remember that BP (blood pressure) = CO (cardiac output) x PR (peripheral resistance)
So, with knowing this, if the RAA alters circulating fluid volume and peripheral resistance we know that RAA directly affects blood pressure.
here is some background information…
Renin is released by the kidneys in response to decreased kidney perfusion. We know that the kidneys receive blood for filtration via the nephron so with decreased vascular fluid volume we will have decreased fluid filtering through the glomerulus and as a result, an overall decreased fluid/blood perfusion to the kidneys leading us to the stimulation of renin.
Angiotensin I and Angiotensin II
Renin causes the release of angiotensin I. Angiotensin converting enzyme (ACE) converts angiotensin I into angiotensin II where angiotensin II is a powerful vasoconstrictor. Therefore, the vasoconstrictor effect that angiotensin II has causes changes in peripheral resistance.
Angiotensin II causes the release of aldosterone from the adrenal cortex. Aldosterone is an important player in the regulation of sodium and water. Aldosterone causes the reabsorbtion of sodium in the distal convoluted tubules, thereby creating a concentration gradient resulting in water retention. The result is an increase in circulating fluid volume, an increase in fluid to the heart and therefore an increase in cardiac output.
Also what is very interesting is that Anti-diuretic Hormone (released from the hypothalamus to the posterior pituitary gland) is stimulated for release from the high concentrations of sodium in the blood (direct result of aldosterone). ADH will cause water retention and therefore an increased cardiac output.
What does this mean for ACE inhibitors?
ACE inhibitors stop activity very early in the RAA cascade. ACE inhibitors do not allow angiotensin I to ever become angiotensin II, therefore we never experience the vasoconstriction (PR) effects of angiotensin II. We never experience the effects of aldosterone, or ADH (CO) and the end result is decreased blood pressure! Where BP = CO x PR!
Why would one take an ACE inhibitor
People with CHF or with HTN will require ACE inhibitors to either decrease the blood pressure or decrease the workload (specifically the afterload) of the heart (which is the case with CHF). Captopril will also decrease the progression of diabetic nephropathy.
The most obvious side effect is Hypotension. Proteinuria is listed as a GU side effect, as well as renal failure and impotence. Captopril can cause neutropenia which is a very serious side effect and can be life threatening. Hypokalemia (decreased potassium) is also serious because potassium is involved in nerve conduction including the heart. Regular hematology and electrolytes should be done.
Nurses, doctors, pharmacists mainly. The thing is with these drugs, is that they are used a lot. If you are giving an ACE inhibitor have you ever thought to take pre and post blood pressures? Ensuring that the recipient isn't hypotensive is a good idea. On the other hand don't withhold these drugs without consulting a physician.