BP-Florinef

Blood Pressure and Florinef interaction

Richard N. Loeppky

Professor of Chemistry, Emeritus

I would like to try to clarify the florinef-blood pressure issue. The kidney is the organ which acts as the control center for the maintenance of blood pressure. The main function of the kidney is to remove salts and other water-soluble unwanted substances from our body by making urine. The most abundant salt in our body is table salt, sodium chloride. Sodium has many important functions in our body and something has to control how much sodium is excreted by the kidney into the urine it makes. This control function is performed by the adrenal steroid aldosterone. It tells the kidney how much sodium to retain and as sodium is retained so is water. By this means proper blood volume is maintained. Those of us with primary Addisons do not make aldosterone. Without it being replaced by florinef, or without taking any other adrenal steroids (hydrocortisone, prednisone, methylprednisone, or dexamethasone) we would continue to excrete sodium uncontrollably. As a consequence our potassium levels would get higher and higher. We would become dehydrated, have frequent fainting spells, experience severe muscle cramps, have unusual pains, and other symptoms which are associated with severe mineral imbalance. Moreover, we could be close to death as the potassium level climbs higher and higher. I had all of these symptoms prior to dx. Because our sodium and blood volume is low in such circumstances we would have unusually low blood pressure and postural hypotension.

Blood pressure is controlled by a complex system in which the main actors are renin, angiotensin II, and aldosterone. Renin is an enzyme which sets up the manufacture of the main BP controlling hormone, a peptide called angiotensin II. Renin is released by the cells in the kidney. Its release triggers an increase in blood pressure through the synthesis of angiotensin II. Among other very important functions, such as constriction of the blood vessels (vaso-constriction), angiotensin signals the adrenal gland to make more aldosterone, but this cannot happen in those of us with primary Addisons. The signal occurs because the whole system needs enough sodium ions and water to work. In short, aldosterone, and its replacement florinef, do not directly control blood pressure, they are only responsible for providing enough sodium and water retention for the system to function.

The secretion of renin is increased by these factors: low arterial BP, low sodium, high potassium, low aldosterone. It is also responsive to the levels of parathyroid hormone, glucagon, “andrenergic agonists” of which adrenaline is an example, and several other types of molecules (cAMP, prostaglandins), all of which increase renin secretion and increase BP. (This is why I do not believe that renin measurements are a good indicator of whether we are getting enough florinef. There are too many other factors that renin secretion responds to.) There are indications that calcium levels also change renin secretion, but this is not yet clear. Low calcium has been suggested to increase renin secretion and BP.

My opinion bottom line: As long as our sodium levels are not above average, we need not worry about the effect of florinef on blood pressure. It mainly can do this only by increasing the sodium level in our system. Most of us do not have this problem. Blood pressure is mainly controlled by angiotensin.

I hope this is understandable. Remember that I am not a physician.