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."

And we have the presentation from Fluge and Mella:

B-lymfocytt deplesjon og sykdomsmekanismer ved kronisk utmattelsessyndrom/ myalgisk encephalopati (ME/CFS)

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?

H2S is elevated in POTS:

Plasma hydrogen sulfide in differential diagnosis between vasovagal syncope and postural orthostatic tachycardia syndrome in children

Postural orthostatic tachycardia syndrome with increased erythrocytic hydrogen sulfide and response to midodrine hydrochloride

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

Carbon monoxide and hydrogen sulfide: gaseous messengers in cerebrovascular circulation

Involvement of endothelial-derived relaxing factors in the regulation of cerebral blood flow

Further reading:

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