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onsdag den 4. juni 2014

ME/CFS/POTS - decreased bioavailability of NO?

A new interesting POTS article:

Blunted Cerebral Blood Flow Velocity in Response to a Nitric Oxide Donor in Postural Tachycardia Syndrome (POTS): "We conclude based on the current study outcomes decreased bioavailability of NO is apparent in the vascular beds resulting in a down regulation of NO receptor sites, ultimately leading to blunted responses to exogenous NO."


They also mention a hypothesis about NO bioavailability in ME/CFS.

Now, what if, the blunted blood flow results in diminished O2 to the cells - will H2S be elevated as compensation?


And how do CO, NO and H2S work together to regulate cerebrovascular circulation?

Carbon monoxide and hydrogen sulfide: gaseous messengers in cerebrovascular circulation


Hydrogen Sulfide as an Oxygen Sensor

Basic knowledge NO - H(2)S - CO interaction - where to begin

ME/CFS, POTS - carotid body and gasotransmitters

ME, POTS, H(2)S, NO - hvad er sammenhængen?

Hydrogen sulfide, ME/CFS, POTS and TRPA1

Roles of nitric oxide, carbon monoxide, and hydrogen sulfide in the regulation of the hypothalamic–pituitary–adrenal axis

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