NO-sensitive guanylyl cyclase (NO-GC) acts as the receptor for nitric oxide and
by the increase in cGMP executes most of the NO effects in the cardiovascular and neuronal
system. Two isoforms of NO-GC exist whose existence has not been paid much attention to
probably because they reveal comparable regulatory and catalytic properties and therefore
cannot be differentiated in vivo. Analysis of mice in which either one of the isoforms has
been genetically deleted unequivocally establishes the coexpression of NO-GC1 and NOGC2
in any tissue tested to date with the exception of platelets. In tissues other than brain
and platelets, no particular function could be ascribed to a specific NO-GC isoform so far. In
contrast, NO-GC1 and NO-GC2 serve different functions in the central nervous system. With
NO-GC1's presynaptic role and NO-GC2's postsynaptic action, two NO/cGMP pathways
have been shown to exist that enhance the strength of synaptic transmission on either side of
the synaptic cleft.
Keywords: Nitric oxide, cGMP, guanylyl cyclase, knock-out, smooth muscle tone, blood pressure, inhibition of
platelet aggregation, synaptic transmission.
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