AJP - Heart and Circulatory Physiology, Vol 263, Issue 4 1045-H1053, Copyright © 1992 by American Physiological Society
Neuropeptide Y and coronary vasoconstriction: role of thromboxane A2
S. E. Martin, J. T. Kuvin, S. Offenbacher, B. M. Odle and R. E. Patterson
Carlyle Fraser Heart Center, Crawford Long Hospital, Emory University, Atlanta, Georgia.
We previously reported that coronary constriction following neuropeptide Y
(NPY) was alleviated by cyclooxygenase blockade. To determine the role of
thromboxane A2 (TxA2), anesthetized dogs received two paired doses of NPY
given 2 h apart. Nine control dogs received NPY alone. Nine test dogs
received one of three TxA2 receptor antagonists given between the doses of
NPY. Also, five dogs received NPY during which prostaglandins were
measured. In controls, NPY decreased coronary blood flow and increased
aortic pressure; coronary resistance was increased significantly. Heart
rate fell, and myocardial oxygen consumption was unchanged. Thromboxane
receptor blockers significantly relieved the coronary constrictor effect of
NPY. The reduction in coronary blood flow was blunted, while heart rate,
first derivative of left ventricular pressure, and myocardial oxygen
consumption were unchanged. Alleviation by TxA2 receptor blockade
paralleled that reported for cyclooxygenase inhibitors. Also, significant
increases in coronary venous TxA2 were seen at the time of maximal
increases in coronary resistance, while prostacyclin was unchanged. In
summary, TxA2 appears to mediate part of the coronary constrictor effect of
NPY.
