CarolI happen to have saved an old post of Joan W.'s on this subject. I'm sure she won't mind if I replay it here. Thanks, Joan, for sharing with us your encyclopedic knowledge!Here is possibly more than you ever wanted to know about renin, aldosterone, Florinef and how they relate to CAH.Renin is involved in the system that regulates blood volume, blood pressure and electrolyte balance. Plasma renin activity is used to monitor the efficacy of mineralcorticoid replacement (Florinef) therapy in CAH. When blood volume and hence blood pressure drops, renin is released from cells that line small arteries (arterioles) located in the kidneys. The effect of this increased renin is to increase the level of Angiotensin-I in the blood. Renin is not directly measured in the test for plasma renin activity; what is actually being measured is the level of Angiotensin-I. You can find normal levels for the plasma renin test here:
http://www.gla.ac.uk/departments/pathologicalbiochemistry/HANDBOOK/endocrin.htm#renin
Angiostensin-I is converted into Angiotensin-II which causes blood vessels to constrict and stimulates the adrenal glands to produce aldosterone. In CAH, the test for plasma renin activity is a way of determining whether or not the adrenal glands are being stimulated to produce aldosterone. When plasma renin activity is above normal it is an indication that the Florinef dosage is too low.
Aldosterone plays a critical role in maintaining the proper balance of sodium and potassium in the body by causing cells, especially kidney cells, to retain sodium and lose potassium. In CAH, the lack of aldosterone causes the reverse to happen, i.e., sodium is lost and potassium is retained. So, in addition to being regulated by the renin-angiotensin system, aldosterone synthesis is also controlled by the balance of these electrolytes. While low sodium is a modest stimulator of aldosterone synthesis, high potassium is a far more potent stimulator.
Much of what I have said so far can be found in this article on the adrenal glands:
http://www.britannica.com/bcom/eb/article/printable/7/0,5722,108527,00.htmlSo what does this mean in CAH? At first glance it would appear that the lack of either aldosterone or its replacement, Florinef, would be fatal to salt wasters. That would be true were it not for the fact that unrestricted access to salt and water is sufficient to overcome the threats posed by electrolyte imbalance and low blood volume. This is fortunate for me since Florinef was not available until I was in my twenties. As a child I consumed enormous amounts of salt and since this naturally made me very thirsty, my doctor had to provide my school with a letter explaining that for health reasons I needed unrestricted access to the water fountain. Obviously that kind of situation makes Florinef a boon for salt wasters.
In addition to preventing salt wasting, Florinef is beneficial, even to non salt wasters, for another reason. The 21-hydroxylase enzyme that is defective in most cases of CAH (> 90%) is also necessary for aldosterone synthesis. In non salt wasters this enzyme defect is not as severe and sufficient aldosterone can be produced to prevent salt wasting. But this is accomplished by the production of higher than normal amounts of aldosterone precursors (building blocks). Any aldosterone precursors that don't become aldosterone will go into the synthetic pathway that produces androgens. Florinef may thus be prescribed to non salt wasters in order to shut down this inefficient aldosterone synthesis and stop its contribution to androgen excess.
Hope this helps.
Joan