Angiotensin is a protein hormone that causes blood vessels to become narrow. It helps us to maintain blood pressure and fluid balance in the body. I created the below chart several years ago as I realized that angiotensin conversion problems could be the main contributor to hypnic jerking and the issues I was experiencing. The renin-angiotensin-aldosterone system (RAAS) plays an important role in the regulation of blood pressure. Angiotensin II (see in the chart) is the principal hormone in the RAAS, causing vasoconstriction and increased sodium and water retention, leading to increased blood pressure.
If one is to look at angiotensin conversion, they would see that there is a lot of evidence supporting a picture of poor conversion (poor generation of angiotensin) in the case of hypnic jerking. In the box on the left side of the diagram I created below, you can see my symptom list.
You'll then see my evidence that supports the theory:
· Out of range blood levels (lowered ACE, A2, and consistently low ADH)
· Genetic mutations involving calcium and potassium channels (activated channelopathies).
· Infections and toxins (parvovirus, actinomycosis, and mold) found that affect the nasal mucosa.
· Consistently poor perfusion index.
· CSF flow MRI’s substantiating trapped brain fluid.
· Positive response to Diamox (detailed in another blog).
· Consistently lower blood pressure.
Two other points of note:
I believe that in the case of hypnic jerking, there is also a level of structural interference that further exacerbates vasoconstriction issues associated with poor conversion. I am specifically referring to trapped nerves (this can result from issues of hypermobility or spinal damage).
I’m thinking that if bradykinin could be tested, that would be elevated as well (contributing to the “princess and the pea” phenomenon so many of us in the group describe).
Please comment below this blog if any of your testing substantiates the theory.