Rabbit thoracic aorta was used to determine the effects of decreasing
PO2 on the mechanical properties of contractions in response to norepi
nephrine and KCl. Aortae were aerated with 45% O-2/5% CO2/50% N-2 and
stimulated with 10 mu M NE or 50 mM KCI. At 5 min of stimulation, 5% C
O2/95% N-2 aeration was introduced for 15 min, defined as hypoxia. Thi
s time period was previously shown to produce similar decrease in [ATP
] in either stimulation condition. Force, stiffness and isotonic short
ening velocity were monitored during the initial stimulation, during h
ypoxia and during re-oxygenation. Hypoxia produced a substantial and r
apid decrease in force and a concomitant decrease in stiffness during
NE stimulation; delayed and smaller decreases in force and stiffness w
ere observed during KCl stimulation. The force-stiffness relationship
was steeper during KCl than NE stimulation, and hypoxia did not affect
these relationships. Isotonic shortening velocity was significantly d
epressed by hypoxia during both stimulations although the decrease dur
ing KCl stimulation required a longer time. These data demonstrate tha
t relaxation of an agonist-induced contraction in response to hypoxia
results from a decrease in the number of activated crossbridges and no
t formation of rigor bridges.