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Junior Member
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Join Date: Sep 2006
Location: France, Lyon
Posts: 49
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Junior Member
Join Date: Sep 2006
Location: France, Lyon
Posts: 49
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PD and high BP drugs: one train may hide another train
Hello Ron,
........"One train may hide another train..."
When a molecule is prescribed, our attention may be only focused upon the very mechanisms that will lead to positive effects and relief of the pain or sorrow we have been complaining of and it has been indicated for. But however, this active molecule has many other biological effects, usually known and evaluated long before to get the FDA or our european equivalent organisms approvals. And when some of these effects may occur and impair our lives besides the main positive one, as we all know, it may happen too, at times, that their mechanisms fit in a positive way for other health problems we have at same time.
A physician is trained to know all about these good or negative results and chooses the best tablets that will combine effects if they are required.....and gives explanations to his patient about how and why he has made his choice of such a molecule ....
"High BP drugs" ...so much to say...it is hard to know which therapeutic class to start with....
Angiotensin II type 1 receptor blockers ? Angiotensin-converting enzyme (ACE) inhibitors? Calcium channel blockers? Diuretics? Beta-blockers ? Sympathetic nerve inhibitors? Vasodilatators?
As Beta-blockers and Angiotensin II type 1 receptor blockers are very frequently prescribed (and as I have mcuh more ideas about their potential action in PD process than about the other drugs  ), here comes my answer, at least a partial one, to your question.
Beta-blockers
The people you are talking about have not been given any anti-parkinsonian drugs.
This evokes a very mild type of illness with A very slow evolution and, at least statistically, more a form with shivering and without disability.
If I am right, then Beta-blockers may have lessened the tremor enough not to be visible to others....
This is my first -very simple -idea.
Below is a much more complex one, take it as a theorical exercise upon the data you've given.
Angiotensin type-1 receptor (AT1R) blockers (ARBs)
In Parkinson's disease, the massive neuronal cell death occurs as a consequence of an inflammatory response, where activated microglia and their cytotoxic agents play a crucial pathological role.
The immune pattern of PD is the one of a Th1 reaction
Angiotensin type-1 receptor (AT1R) blockers (ARBs)
1/ potentially attenuate lipopolysaccharide-induced neuroinflammation and reduces neuronal death by a mechanism dependent of peroxisome proliferator-activated receptor gamma (PPAR)activation.
2/ may regulate the nitrosative stress-induced apoptotic cell death in contributing to regulated expression of inducible nitric oxide synthase (iNOS) and regulated production of nitric oxide (NO)
3/ may modulate the immune system shift from Th1 inflammatory/autoimmune reactions to Th2 through VDR (vit D nuclear Receptor), PPAR and CCR2b C-C (chemokine receptor type 2)
4/ may cause inhibition of oxidative stress activation as Angiotensin II activates (via type 1 receptors) NAD(P)H-dependent oxidases, which are a major source of superoxide.
In hope for complementary data or contradictory posts to come.
Anne.
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