Midrodrine or ProAmatine is vasopressor/antihypotensive drug approved for use in the U.S. for the treatment of dysautonomia and orthostatic hypotension. It works by producing a metabolite which activates alpha-adrenergic receptors found in arteries and veins which then constrict the blood vessels causing an increase in blood pressure.
The Light's work at the University of Utah suggests alpha adrenergic receptors could play a significant role in some chronic fatigue syndrome (ME/CFS) patients.
Because midodrine's effects are short-lived, midodrine usually must be taken several times a day. Because Midodrine increases in blood pressure about four hours after taken it should be taken at least 4 hours before going to bed. Cold remedies that can increase blood pressure should be used with caution as well. Dr. Klimas suggests taking Midodrine before meals.
Doses generally start out low (2.5 mg) and increase over time (2.5-10 mg three times a day).
Midodrine and Chronic Fatigue Syndrome (ME/CFS)
A 2004 report by Naschitz, an Isreali researcher, concerning one patient found that Midrodrine corrected the his dysautonomia and improved his fatigue. No followup studies, unfortunately, have been done.
Dr Chia and Dr. Klimas reported successfully using Midodrine in some ME/CFS patients. At the 2008 IACFS/ME conference Dr. Bell stated he’d used Midodrine effectively in many patients. Similarly, Dr. Rowe has reported success as well.
One interesting Midodrine story involved an ME/CFS patient without POTS or orthostatic hypotension but with symptoms of dysautonomia whose fatigue improved by 40%, whose mental clarity improved so much that it shocked him, and who is able to withstand many more stressors without problems.
Dr. Rowe reported that ME/CFS patients with orthostatic hypotension (low blood pressure on standing) can experience high blood pressure when lying down, itching, pins and needles sensations and urinary urgency when taking Midrodrine.
Midrodrine and Postural Orthostatic Tachycardia Syndrome (POTS)
Midodrine's effects in postural orthostatic tachycardia (POTS) are well-established. A large (n=104) retrospective 2014 study in children with POTS suggested that Midodrine was effective in raising their blood pressure when standing. Another 2014 study suggested that Midrodrine was effective in decreasing the capacity of the veins to carry blood (it reduced blood pooling in the limbs) in neuropathic but not hyperadrenergic POTS. (Vasoconstricted blood vessels are already present in hyperadrenergic POTS patients.)
Laio found reduced symptom scores and reduced heart rate increases during a tilt table test in a large (n=138) POTS study. Li found that measuring plasma coeptin allowed him to identify Midodrine responders in POTS patients. Chen found that midrodrine was more effective than conventional therapy in POTS patients.