To test the hypothesis that
prostanoids contribute to
angiotensin II-induced vascular contraction, we compared the effect of
angiotensin II on isometric tension development by rings of descending thoracic aorta bathed in Krebs'
bicarbonate buffer with and without
indomethacin (10 microM) to inhibit
cyclooxygenase, CGS13080 (10 microM) to inhibit
thromboxane A2 synthesis, or SQ29548 (1 microM) to block
thromboxane A2/
prostaglandin endoperoxide receptors. The comparisons were made in rings of aorta taken from normotensive rats and from rats with
aortic coarctation-induced
hypertension at 12 days and 90-113 days after coarctation. These rings released
thromboxane B2, which was found to be endothelium dependent, increased in hypertensive rats, and stimulated by
angiotensin II (10(-6) M) in normotensive rats and in hypertensive rats at 12 days after coarctation. The
angiotensin II (10(-6) to 10(-5)M)-induced contraction of aortic rings was increased by about 30% at 12 days after coarctation and decreased at 90-113 days after coarctation. Removal of the endothelium increased the contractile effect of
angiotensin II (10(-6) M) in aortic rings of normotensive rats and hypertensive rats at 90-113 days after coarctation but decreased the effect in aortic rings of hypertensive rats at 12 days after coarctation. In rats at 12 days after coarctation, the
angiotensin II (10(-6) M)-induced contraction of aortic rings with endothelium was attenuated by
indomethacin and SQ29548 but not by CGS13080. These data suggest that a
prostanoid-mediated and endothelium-dependent mechanism of vasoconstriction contributes to the constrictor effect of
angiotensin II in aortic rings of rats in the early phase of
aortic coarctation-induced
hypertension.