L2 - rfr_id=ori:rid:&rfr_dat=cr_pub=pubmed Short-term ET-receptor inhibition in experimental hypercholesterolemia attenuated the enhanced coronary epicardial vasoconstrictor effects of ET-1 but not acetylcholine-induced coronary epicardial vasoconstriction, suggesting that acetylcholine-induced coronary epicardial vasoconstriction may not be mediated by ET receptors. Bosentan did not affect the response to acetylcholine at baseline or 10 weeks. FR-139317 did not affect the response to acetylcholine at baseline (%deltaCAD 5+/-2% for group III versus 7+/-3% for group IV, P=NS) or at 10 weeks (%deltaCAD -23+/-12% for group III versus -19+/-7% for group IV P=NS). FR-139317 did not attenuate the epicardial vasoconstrictor response to ET-1 at baseline (%deltaCAD -18+/-8% for group I versus -12+/-6% for group II P=NS) but did at 10 weeks (%deltaCAD -77+/-14% for group I versus -14+/-6% for group II P<.05). Sarafotoxin 6c mildly reduced %deltaCAD at baseline and 10 weeks (-10+/-2% and -12+/-3%, respectively). The percentage change in coronary artery diameter (%deltaCAD) to the infusions was measured at baseline and after 10 weeks of high-cholesterol diet in all animals. The ETB-receptor agonist sarafotoxin 6c (5 ng x kg x min n=4) was also infused.
#Deltacad free plus#
Acetylcholine was also infused with the combined ET-receptor blocker, bosentan (0.5 mg/kg plus 1 mg x kg x h, group V, n=5). ET-1 and acetylcholine were also infused with the specific ETA-receptor blocker FR-139317 (5 microg x kg x min group II, n=6 group IV, n=6). ET-1 (group I, n=5 5 ng x kg x min) and acetylcholine (group III, n=7 10 to 10 mol/L) were given by intracoronary infusion in pigs. We hypothesized that short-term inhibition of ET receptors attenuates the coronary epicardial vasoconstrictor response to acetylcholine in experimental hypercholesterolemia. N2 - Endothelin (ET) may mediate the enhanced coronary vasoconstriction associated with hypercholesterolemia. JF - Arteriosclerosis, thrombosis, and vascular biology T1 - Acute endothelin-receptor inhibition does not attenuate acetylcholine-induced coronary vasoconstriction in experimental hypercholesterolemia.
Endothelin (ET) may mediate the enhanced coronary vasoconstriction associated with hypercholesterolemia.