Prostaglandins in carotid sinus enhance baroreflex in rabbits.

The purpose of this study was to examine the possible influence of endogenous prostaglandins in the carotid sinus on the arterial baroreflex. Lumbar sympathetic nerve activity (LSNA) and arterial pressure were recorded during step increases in isolated carotid sinus pressure in rabbits anesthetized with chloralose. Baroreflex responses were facilitated after intrasinus administration of prostacyclin (PGI2; 5 and 10 microM, n = 6) or arachidonic acid (10 microM, n = 12). PGI2 (10 microM) increased the slope of the carotid sinus pressure-LSNA relation (gain) from -0.32 +/- 0.09 to -1.19 +/- 0.38 spikes.s-1.mmHg-1 and decreased the pressure at which 50% of the maximum inhibition of LSNA occurred (EP50) from 127 +/- 5 to 98 +/- 4 mmHg (P less than 0.05). Similar responses were observed with arachidonic acid. Baroreflex responses were attenuated after intrasinus administration of indomethacin (40 and 80 microM, n = 5) or aspirin (1 and 2 mM, n = 7). Indomethacin (80 microM) decreased the gain of the baroreflex from -1.02 +/- 0.24 to -0.47 +/- 0.16 spikes.s-1.mmHg-1 and increased the EP50 from 121 +/- 6 to 133 +/- 7 mmHg (P less than 0.05). Both indomethacin (80 microM) and aspirin (2 mM) reduced the maximum percent inhibition of LSNA significantly. The results indicate that prostaglandins within the carotid sinus facilitate the baroreflex control of LSNA. The attenuation of the baroreflex after inhibition of cyclooxygenase suggests that endogenous prostaglandins contribute to the activation of baroreceptors during increases in carotid sinus pressure.