Why gaseous nitric oxide inhalation does not influence on systemic arterial pressure in human and animal organisms?

The reason has been elucidated why gaseous nitric oxide inhalation does not produce hypotensive effect in human and animal organisms. The defect was completely removed when low molecular thiol solutions were added by intravenous pathway simultaneously with gaseous NO inhalation into the animals (rats). The proposition was made that gaseous NO molecules including through the lungs into the circulation of the blood are transformed as a result of one-electron mechanism oxidation into nitosonium cation (NO+) which are not capable of vasodilating and thereby hypotensive action on men and animals. NO+ cation binding with low molecular thiols results in the S-nitrosothiol (RS-NO) formation with following release of the nitrosyl component from the RS-NO in the form of neutral NO molecule characterized with hypotensive activity. The formation of another NO donor - dinitrosyl iron complexes with thiol-containing ligands did not occur in the animals. Hypotensive action observed in lungs could be determined by gaseous NO penetration trough external vascular wall followed by the activation of vasodilation and hypotensia inductor - guanylate cyclase enzyme immediately inside of vascular walls.

Gaseous nitric oxide, inhalation, hypotensia, Nitrosonium cation, S-mitrosothiols