ace inhibitors

[popeye77]

Anybody take Lotensin or Accupril? I started on 10mg per day about 8 yrs ago. About 4 yrs ago went to 20 mg. As of one month ago I was prescribed 40 mg. per day which brought my diastolic down from around 95 to 85. I am admittedly about 45 lbs. overweight (but I'm big boned .....Ha Ha) I'm trying to work on the weight but at 58 it's tough. So much for background. 40 mg. of Lotensin or Accupril gives me headaches and dizzyness to the point I have a tough time driving. So I cut back to 20 mg. in the a.m. and carry extra 20's in case I feel BP rush later in the day. What do you think of breaking 40 mg pills in half? Does that allow too much of "time release" med when initially taken. I guess I'm asking do most think ACE inhibitors are effective?

[Palamedes]

Originally Posted by jrmcxx

What do you think of breaking 40 mg pills in half? Does that allow too much of "time release" med when initially taken.

No problem. These aren't really "time release" meds. They just get in your bloodstream and get eliminated over time.

I guess I'm asking do most think ACE inhibitors are effective?

One of the key things to realize with ACE inhibitors and ARBs is that they only work effectively if your keep your sodium consumption reasonable. If you consume lots of sodium, the drug does absolutely nothing. The more you restrict sodium, the better it works.

If you can't keep your sodium under control, then you need to combine it with a diuretic which WILL keep your sodium under control. That's why the two drugs combine so well. The diuretic (or a sodium restricted diet) reduces volume. Reducing volume SHOULD cause your BP to drop. However, our bodies have developed a feedback mechanism that kicks in so BP doesn't drop. The ACE inhibitor blocks this feedback allowing the diuretic (or low sodium diet) to do it's job.

Pal

[CASSIEBEL]

If you can't keep your sodium under control, then you need to combine it with a diuretic which WILL keep your sodium under control. That's why the two drugs combine so well. The diuretic (or a sodium restricted diet) reduces volume. Reducing volume SHOULD cause your BP to drop. However, our bodies have developed a feedback mechanism that kicks in so BP doesn't drop. The ACE inhibitor blocks this feedback allowing the diuretic (or low sodium diet) to do it's job.

Pal,
You seem to know a lot about these meds. Do you know if one, (ARB or ACEI) works better than the other when combined with a diuretic?
Just curious.
Cass

[Lenin]

jrmcxx,
There is a tendency for the body to "get used" to the ACE inhibitor class of BP meds over several months. The cause seems to be other methods that ultimately produce Angiotensin 2 in the same quantity as before. ACE is responsible for about a quarter of the Angiotensin 2 production, chymase conversion is the other 3/4 and that mechanism ramps up in response to the fall in ang2.
That explains the rather normal routine of starting at 10, going to 20 and then to 40 mg. that you went through.
It might be time for a new drug class, perhaps an angiotensin receptor blocker (ARB.)

I've found the same thing that PAL found: that ARB's (and by extension ACEI's) are not much use without salt restriction or diuretics.

[Palamedes]

Originally Posted by CASSIEBEL

Do you know if one, (ARB or ACEI) works better than the other when combined with a diuretic?

I would expect similar results. However, from a purely scientific point of view, it would seem logical that the ARB might show more of a dependency on a diuretic (or low sodium diet) than the ACEI. This is probably splitting hairs. But, the reason I would make that guess is that an ACEI has another mechanism by way of increasing bradykinin levels. This also helps reduce BP slightly - though, this is not as significant as reducing ang II. However, bradykinin is a two edged sword as it also causes the cough.

Also, Lenin brought up a very good point. There is a lot of scientific evidence that the non-ACE pathways can actually cause ang II levels to return to normal over time. Thus, the potency of the ACEI can degrade. I should also add that there is another pathway called "tissue plasminogen activator" (tPA) that can also convert directly from angiotensinogen straight to ang II - bypassing renin, ang I and ACE altogether.

In the next couple years, we'll get yet another class called "Renin Inhibitors" (RI). The initial trials are showing these to have very good side-effect profiles (similar to ARBs). This should take care of the chymase pathway. But, it won't do anything for the tPA. I suspect the ideal future combo will be a RI + ARB. Though expensive, this should provide a near 100% blockage with virtually no side-effects.

Today, the ACE + ARB combo is very potent. But, side-effects can get out of hand - bradykinin levels get even higher. Speaking of which, there is another class called vasopeptidase inhibitors (aka. Super ACEI). While they are very potent, they have similar problems to the ACE + ARB combo. So much so, the FDA most likely will never approve this class.

Oh well... I need to stop. I am getting carried away here.

Pal