Opposition of rapid baroreceptor resetting by prostanoids in rabbits

Arterial baroreceptors reset rapidly within minutes during acute hypertension; baroreceptor pressure threshold (Pth) is increased and the pressure-baroreceptor activity relation is shifted to the right. The purpose of the present study was to determine if prostacyclin (PGI2) or other prostanoids, released during acute hypertension modulate the magnitude of baroreceptor resetting. Baroreceptor activity was recorded from the vascularly-isolated carotid sinus during distension of the sinus with slow pressure ramp in rabbits anesthetized with chloralose. Pressure-activity curves were generated after holding carotid sinus pressure for 10-15 min from 30 to 100 mmHg. In control, the elevation of holding pressure increased Pth from 44+/- to 65+/-5 mmHg (p < 0.05, n = 12). In the presence of PGI2 (20 microM), Pth averaged 43+/-4 and 45+/-3 mmHg (n = 12) after holding pressure at 30 and 100 mmHg, respectively. In the control group before exposing the carotid sinus to indomethacin, an elevation of holding pressure increased Pth from 49+/-2 to 71+/-3 mmHg (p < 0.05, n = 12). After inhibition of the endogenous formation of prostanoids with indomethacin (20 microM), Pth increased by a significantly greater extent from 61+/-2 to 90+/-3 mmHg (p < 0.05, n = 12) with the increase in holding pressure. The slope of the pressure-activity curve (baroreceptor gain) was not influenced by the change in holding pressure. It was increased significantly by PGI2, while decreased by indomethacin. Neither the change in holding pressure nor PGI2 affected the circumferential wall strain of carotid sinus over a wide range of pressure alteration. The results suggest that PGI2 or other prostanoids released during acute hypertension sensitizes baroreceptors and provides a negative feedback mechanism that opposes and limits the magnitude of rapid baroreceptor resetting.