1 Nitrovasodilators produce characteristic changes in the shape of the peri
pheral pulse wave. Similar changes might also be caused by alteration of en
dogenous NO activity, which would allow such activity to be assessed in viv
o.
2 We investigated whether manipulation of the NO pathway influences the pul
se waveform, and the mechanisms involved. The pulse wave in the ear of norm
al rabbits was examined by reflectance photoplethysmography before and duri
ng infusion of vasoactive agents. Pulse wave velocity was assessed by using
on additional sensor on the rear foot.
3 A diastolic peak was observed in the ear pulse; its timing was consistent
with it being a reflection of the systolic peak From the lower body. The h
eight of the dicrotic notch marking the start of this diastolic wave was de
creased by acetylcholine or an NO donor, and further decreased by a phospho
diesterase type V inhibitor. The acetylcholine-induced decreases were block
ed by inhibiting NO synthesis with N-G-nitro-L-arginine methyl ester (L-NAM
E) but were unaffected by the inactive enantiomer D-NAME.
4 These data demonstrate that NO influences the height of the notch in the
pulse wave. Heart rate and blood pressure were altered during acetylcholine
or L-NAME infusion, but there were no changes in pulse wave amplitude or v
elocity, or in the timing of the diastolic peak or dicrotic notch. The slop
e of the pulse wave between the systolic peak and notch changed substantial
ly. These effects are most convincingly explained bq changes in wave reflec
tion, not only from the lower body but also from more proximal sites.