Baroreflex inhibition during coronary occlusion is mediated by prostaglandins

Irving H Zucker, M. J. Panzenbeck, J. F. Hackley, K. Haiderzad

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16 Citations (Scopus)

Abstract

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- and 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.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume257
Issue number1
StatePublished - Jan 1 1989

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Baroreflex
Coronary Occlusion
Prostaglandins
Indomethacin
Dogs
Kidney
Arterial Pressure
Coronary Vessels
Thorax
Nitroprusside
Prostaglandin-Endoperoxide Synthases
Ischemia

ASJC Scopus subject areas

  • Physiology

Cite this

Baroreflex inhibition during coronary occlusion is mediated by prostaglandins. / Zucker, Irving H; Panzenbeck, M. J.; Hackley, J. F.; Haiderzad, K.

In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 257, No. 1, 01.01.1989.

Research output: Contribution to journalArticle

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