PGI2 attenuates baroreflex control of renal nerve activity by a vagal mechanism

The present study was undertaken to determine whether left circumflex coronary artery (ic) administration of prostacyclin (PGI2) caused an inhibition of the baroreflex control of renal sympathetic nerve activity (RSNA). RSNA was recorded in 12 dogs. Baroreflex sensitivity of RSNA was assessed by infusion of either sodium nitroprusside or phenylephrine and by determining the slope of the mean arterial pressure-RSNA relationship. During nitroprusside infusion, intracoronary PGI2 depressed the baroreflex sensitivity by nearly 90% compared with intracoronary tris(hydroxymethyl)aminomethane (Tris) (P less than 0.002). In addition, the peak increase in RSNA during nitroprusside infusion was significantly inhibited during intracoronary PGI2 (57.9 +/- 6.4 vs. 21.2 +/- 3.0 spikes/s, P less than 0.05). There was no significant difference in the inhibition of RSNA during phenylephrine infusion when intracoronary PGI2 was compared with Tris. Both bilateral vagotomy and pericoronary lidocaine blocked the inhibitory effects of PGI2 on the baroreflex increase in RSNA. It is concluded from these data that exogenously administered PGI2 stimulates or sensitizes afferent endings within the supply of the left circumflex coronary artery to inhibit the baroreflex control of RSNA during evoked hypotension. These afferents traverse vagal pathways via the pericoronary nerves. The role of endogenous prostaglandins in modulation of baroreflex function via a cardiac reflex remains to be elucidated.