Double-Duty Drug

Antihypertensive drug shows benefit for multiple sclerosis

(RxWiki News) A drug designed to lower hypertension has also been found to keep inflammation from multiple sclerosis (MS) in check.

Researchers have discovered a new signaling pathway of brain cells, which may explain how the antihypertensive drugs keep MS inflammation under control. The peptide known as angiotensin elevates blood pressure in addition to activating the immunological messenger substance TGF beta on a previously unknown communication pathway in the brain, according to researchers.

Under normal circumstances, the kidneys use a chemical pathway called the renin-angiotensin-aldosterone axis to increase blood pressure. When blood pressure is low, sensors in the kidney secrete a molecule called renin, which in turn causes the body to secrete angiotensin I. Angiotensin I is converted to angiotensin II, which in turn causes blood vessels to constrict and raise blood pressure.  Angiotensin II also stimulates the production of a molecule called aldosterone, which works on the kidneys to raise blood pressure even more, by reabsorbing sodium and in turn, water into the blood.  

In hypertensive patients, this chemical pathway can be muted by drugs called Angiotensin Receptor Blockers (ARBs), which block angiotensin II receptors in the blood vessels, and prevent constriction of blood vessels that would raise blood pressure.

That means drugs that block the angiotensin receptors -- which have also been found on numerous organs and cells unrelated to blood pressure-control, such as immune system T cells -- may also work for autoimmune reactions such as MS. MS occurs when inflammation in the brain and spinal cord destroys the myelin sheath that covers nerves, which can lead to paralysis and other neurological symptoms.

Dr. Michael Platten of Stanford University in California said since AT1R blockers are frequently prescribed for lowering blood pressure and have been proven safe, the next obvious step is to test them soon in MS patients.


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Review Date: 
December 28, 2010