The regulation of pulmonary vascular tone by acetylcholine (ACh) involves t
he activation of different subtypes of muscarinic receptors as well as the
cholinesterase activities which are responsible for ACh degradation. Most o
f the studies on the cholinergic control of the pulmonary vascular tone hav
e been performed in vessels derived from animals. The ability of ACh to ind
uce pulmonary vasoconstriction is species dependent. In vessels derived fro
m sheep lung, ACh induced contractions in veins but not in arteries whereas
in human pulmonary vessels the reverse was observed. The subtype(s) of the
muscarinic receptors involved in the pulmonary vasoconstrictions is also d
ependent on the species which are studied. M-1 receptors are implicated in
the rabbit pulmonary vasoconstrictions, M-3 in humans, whereas M-1 and M-2
receptors are involved in the dog. The cholinesterases are implicated in th
e vasoconstriction produced by ACh in human and rabbit pulmonary arteries.
However, in these studies while acetylcholinesterase (EC 3.1.1.7) and butyr
ylcholinesterase (EC 3.1.1.8) activities were detected in human vessels onl
y acetylcholinesterase activity was found in rabbit vessels. The endotheliu
m-dependent relaxation induced by ACh has been reported in isolated pulmona
ry vessels from different animals including man. However, the muscarinic re
ceptors involved in the ACh-induced vasodilatation of rat and rabbit pulmon
ary artery are of the M-3 subtype while those characterized in the human pu
lmonary artery are of the Ms and M-1 subtypes. Together these results conce
rning the cholinergic control of the pulmonary vascular tone indicate that
extrapolation of the data obtained in animal models to human vessels requir
es some caution. In addition, there is considerable evidence to demonstrate
that ageing may modify cholinergic responses. However, little information
is available concerning the pulmonary vascular bed during ageing.