Dr. Richard Bruno is Chairperson of the International Post-Polio Task Force and director of The Post-Polio Institute and International Centre for Post-Polio Education and Research at Englewood (NJ) Hospital and Medical Center. His new book, How to STOP Being Vampire Bait: Your Personal Stress Annihilation Program, will be published in 2004. E-mail him at ppsforum@newmobility.com.

Note: This column is for information purposes only and is not intended as a substitute for professional medical advice.

With the holidays coming and bringing their extra load of stress (read: relatives), now is a good time to talk about controlling high blood pressure. As with all things post-polio, there are special considerations when choosing hypertension medications. Physicians typically become comfortable with and use just a small number of medications. The problem is that drugs doctors may regularly use to treat high blood pressure can be problematic for polio survivors.

For years, the first drug prescribed to treat hypertension would be a diuretic, a "water pill." Diuretics, like Diazide and Furosemide, lower blood pressure by decreasing the amount of fluid in your arteries, like taking water out of an overly full balloon. But, diuretics decrease fluid by making you pee ... and pee and pee. Frequent trips to the bathroom may not be an issue for other folk. But it's not a good idea for polio survivors with fatigue and weaker arms and legs to be running (or rolling) to find the nearest accessible bathroom and getting on and off the throne a dozen times throughout the day and night.

Another older antihypertensive is the beta blocker, Inderal being the granddaddy of the group, which blocks adrenaline from stimulating the "beta" receptor on the heart muscle, thereby decreasing the speed and force with which your heart beats. The problem is that these drugs block adrenaline from stimulating beta receptors in other places, including the brain, and thereby decrease brain activation. Polio survivors, especially those with fatigue, don't need a drug that further reduces brain activation. Of all the antihypertensives, beta blockers are probably the worst at producing fatigue as a side effect. In the drug companies' own studies for medications currently listed in the Physicians Desk Reference, fatigue was a side effect in 2 percent to 6 percent of subjects on beta blockers Naldolol, Tenormin or Timolol, versus about 1 percent to 5 percent of those taking a placebo. What's more, Timolol caused cold hands and feet--a symptom polio survivors need no help in developing--in 8 percent of subjects versus 1 percent of those given placebo. Beta blockers can also worsen asthma symptoms.

Other older antihypertensives that cause fatigue are alpha blockers. These drugs stop adrenaline from stimulating the "alpha" receptors on blood vessels and thereby allow arteries to open, lowering pressure by increasing the size of the "pipes" blood can flow through, just as using a bigger hose will reduce the pressure of water flowing out of it. But, as with beta blockers, anything that blocks the stimulating effects of adrenaline can cause brain "deactivation" and fatigue. Fatigue was reported in more than 7 percent of subjects taking alpha blockers Cardura, Hytrin and Minipress, versus 2 percent to 3 percent of those on placebo.

Over the years, newer antihypertensives were developed that don't block adrenaline and are less likely to cause fatigue. The calcium-channel blockers open blood vessels and reduce the force of contraction of the heart by reducing the flow of calcium into muscle cells. CCBs Procardia and Norvasc caused fatigue in from 4 percent to 6 percent of subjects, versus 3 percent to 4 percent of those given placebo.

But, fatigue was not reported with CCBs Cardene and Verapamil. Differences in the ability to produce fatigue were seen among another class of newer antihypertensives, the angiotensin receptor blockers. These drugs prevent angiotensin, a hormone that causes blood vessels to narrow, from stimulating arteries and making them constrict. ARBs Diovan and Avalide caused fatigue in 4 percent to 5 percent of subjects, versus 1 percent to 3 percent of those on placebo. Fatigue was not reported with ARBs Atacand, Micardia, and Cozar.

A varying ability to produce fatigue was also seen among a related group of antihypertensives, the angiotensin converting enzyme inhibitors, which block the production of angiotensin. ACE inhibitors Accupril, Lotensin, Vasotec and Zestril were found to cause fatigue in 2-5 percent of subjects, versus 1 percent to nearly 3 percent of those given placebo. However, fatigue was not reported with ACE inhibitors Aceon, Altace and Monopril.

Considering their side effects, should polio survivors never take certain of these antihypertensives and always ask to use others? We'll answer that question next month.