You are welcome. CCB stands for a calcium channel blocker. It is a cardiovascular drug.
I've been reading about ACE inhibitors and their role in inflammation and turned up some interesting facts, enough for a new thread. (just kidding!
) I'll quickly mention the following, because it relates to what's already been discussed in this thread.
ACE inhibitor blood levels decrease significantly toward the end of the dosing period. This can leave us, the patients, very vulnerable early in the morning when blood pressure tends to rise and the protection is needed the most.
Two factors are important for prolonging functional angiotensin converting enzyme inhibition -the inhibitor-binding affinity and tissue retention. Both influence the ACE inhibitor concentration in the tissue. ACE inhibitors are rated according to their potency, tissue affinity, and how well they dissolve in lipids (fat). It is these properties that determine the antiatherosclerotic effects of different ACE inhibitors and how well they penetrate the atherosclerotic plaque. In clinical trials, high tissue affinity ACE inhibitors -perindopril, quinapril and ramipril- were used.
Increasing the ACE inhibitor dose extends duration of response without altering the peak effect. Many individuals benefit from taking two
daily doses of this drug. Interestingly, ACE inhibitors reduce Angiotensin II levels only in the short term. With chronic use of this drug, Angiotensin II levels return to normal. This means that, besides the angiotensin converting enzyme inhibition, OTHER mechanisms of blood pressure lowering are also in place.
How are you doing? Is the ACE inhibitor keeping your blood pressure controlled? When do you take it?