Coronary reactivity to
endothelin-1 and
vasopressin during acute, moderate
hypertension, and the role of
nitric oxide (NO) and
prostanoids in this reactivity was examined in anesthetized goats. Left circumflex coronary flow was electromagnetically measured, and
hypertension was induced by constriction of the thoracic aorta in animals nontreated (7 goats) or treated with the inhibitor of NO synthesis Nw-nitro-
L-arginine methyl esther (
L-NAME, 6 goats) or the
cyclooxygenase inhibitor meclofenamate (6 goats). Under normotension (19 animals), basal mean values for mean arterial pressure and coronary vascular conductance (CVC) were 89+/-3 mm Hg and 0.36+/-0.038 ml/min/mm Hg, respectively.
Endothelin-1 (0.01-0.3 nmol) and
vasopressin (0.03-1 microg) dose-dependently decreased CVC, which, for
endothelin-1 ranged from 5+/-1% (0.01 nmol; P<0.01) to 66+/-4% (0.3 nmol; P<0.001) and for
vasopressin ranged from 9+/-1% (0.03 microg P<0.01) to 41+/-3% (1 microg; P<0.001). During nontreated and treated
hypertension, mean arterial pressure increased to approximately 130 mmHg (P<0.01), and CVC decreased (17%) only during
L-NAME-treated
hypertension. The effects of
endothelin-1 and
vasopressin on CVC were decreased by approximately 50% during nontreated
hypertension, and this was abolished by
L-NAME and was not affected by
meclofenamate. Therefore, during acute, moderate
hypertension, the coronary vasoconstriction to
endothelin-1 and
vasopressin is attenuated, which may be related with increased NO release but not with
prostanoids.