Conscious rats exposed to 5 bar (500 kPa) ambient pressure show increa
sed total myocardial blood flow (TMBF) and enhanced cardiac contractil
ity in spite of unaltered mean arterial pressure (MAP), heart rate (HR
), and cardiac output (GO). Four groups of awake, adapted rats were gi
ven injections of atenolol at 1 bar air or 5 bar normoxic N-2, or both
. Atenolol injected at 1 bar caused a marked reduction of HR, MAP, pea
k left ventricular pressure (LVP), and rate of LVP rise (+dP/dt) and f
all (-dP/dt). In spite of beta(1)-adrenoceptor blockade, ambient press
ure rise increased HR, LVP, +dP/dt, -dP/dt, TMBF, and calculated cardi
ac O-2 consumption (P < 0.05). A second atenolol injection at 5 bar ca
used a brief reduction in HR but did not affect cardiac contractility.
Rats receiving the first atenolol injection at 5 bar demonstrated unc
hanged TMBF. We conclude that beta(1)-adrenoceptor blockade does not a
nnul the increase in cardiac contractility associated with hyperbaria.