The acute effects of the inhaled gas phase of cigarette smoke on pulmo
nary (PAP) and systemic (SAP) arterial pressures and on plasma arteria
l cGMP content were compared with those of inhaling 10, 20 and 80 ppm
nitric oxide (NO) in one healthy adult volunteer spontaneously breathi
ng a hypoxic gas mixture. Hypoxia (FIO2 0.12) induced a sustained, sta
ble pulmonary vasoconstriction. Inhaled NO induced a dose-dependent fa
ll in PAP; plasma cGMP rose from 39.4 (hypoxia) to 164 pmol/ml (hypoxi
a plus 80 ppm NO). Exposure to cigarette smoke induced a rapid, consis
tent and reversible fall in PAP; plasma cGMP rose from 45.5 (hypoxia)
to 138 pmol/ml (hypoxia plus cigarette smoke). Neither NO nor cigarett
e smoke inhalation induced any change in SAP. These data suggest that
exposure to cigarette smoke is able selectively to reverse acute hypox
ic vasoconstriction in humans without causing systemic vasodilation, a
n effect likely mediated through the NO-cCMP pathway.