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Am J Physiol. 1989 Jul;257(1 Pt 2):R216-23.

Baroreflex inhibition during coronary occlusion is mediated by prostaglandins.

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  • 1Department of Physiology and Biophysics, University of Nebraska, College of Medicine, Omaha 68105.


The present study was undertaken to determine whether the baroreflex control of renal sympathetic nerve activity (RSNA) was attenuated by an acute coronary artery occlusion and if so, what was the role played by cardiac prostaglandins in this attenuation. Arterial pressure was lowered with an infusion of sodium nitroprusside before and during a 5- to 10-min occlusion of the left circumflex coronary artery. The protocol was repeated 30 min after indomethacin (5 mg/kg) had been given. In addition, this study was carried out in a group of vagotomized dogs and in a group of thoracic-sympathectomized dogs. In intact dogs, coronary occlusion reduced the slope of the mean arterial pressure-RSNA relationship by 75% from -7.7 +/- 1.8% change in RSNA per millimeter Hg before indomethacin treatment. After indomethacin, there was no inhibition of the baroreflex slope during coronary occlusion. The reduction in the slope during coronary occlusion was abolished in dogs that were vagotomized but preserved in thoracic-sympathectomized dogs. In this latter group, indomethacin inhibited the attenuation of the slope during coronary occlusion. These data provide strong support for the notion that some cyclooxygenase product (most likely a prostaglandin) is released during coronary ischemia and stimulates or sensitizes cardiac vagal afferent endings, which, in turn, attenuate the baroreflex-mediated increase in RSNA during lowered arterial pressure.

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