U. Lang et al., ESTROGEN-INDUCED INCREASES IN CORONARY BLOOD-FLOW ARE ANTAGONIZED BY INHIBITORS OF NITRIC-OXIDE SYNTHESIS, European journal of obstetrics, gynecology, and reproductive biology, 74(2), 1997, pp. 229-235
Objective: Estrogen receptors have been found in coronary arterial end
othelial and vascular smooth muscle cells. Therefore the present study
was designed to determine if estradiol-17 beta can increase coronary
blood flow and if so whether the changes are mediated by nitric oxide.
Study design: Five oophorectomized non-pregnant sheep were chronicall
y instrumented to measure blood pressure, heart rate, cardiac output,
left circumflex coronary blood flow and central venous pressure. Anima
ls received estradiol-17 beta (1.0 mu g/kg) and cardiovascular respons
es were followed for 135 min. Results: Estradiol-17 beta (1.0 mu g/kg)
increased left circumflex (coronary) blood flow 28+/-3%, cardiac outp
ut 15+/-1% and heart rate by 13+/-3%. Coronary vascular resistance dec
reased 231+/-5%, systemic vascular resistance decreased by 12+/-2% whi
le blood pressure did not change significantly. Administration of the
nitric oxide synthetase inhibitor L-nitroarginine methylester (L-NAME)
, had no effect on basal coronary blood Bow but completely reversed es
tradiol-17 beta induced increases in coronary blood flow. Conclusion:
These results demonstrate that estrogen increases coronary blood flow
in the non-pregnant sheep and that L-NAME, an inhibitor of nitric oxid
e, is able to reverse the estrogen induced flow changes. (C) 1997 Else
vier Science Ireland Ltd.