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      Prostanoids Contribute to Endothelium-Dependent Coronary Vasodilation in Guinea Pigs


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          This study characterizes the contribution of prostanoids to endothelium-dependent responses in two vascular regions of the guinea pig. We compared the mechanisms of relaxation responses to acetylcholine and adenosine triphosphate (ATP) in the coronary vasculature and in the abdominal aorta of the guinea pig. Endothelium-dependent responses were examined in an isolated, potassium-arrested guinea pig heart utilizing a modified Lan-gendorff preparation. Coronary vessels were constricted with prostaglandin F<sub>2α</sub> and dilated with acetylcholine (10<sup>–9</sup>10<sup>–6</sup> mol) or ATP (10<sup>–10</sup>–10<sup>–7</sup> mol) before and after exposure to indomethacin (14 µ M, n = 6) or ibuprofen (150 µ M, n = 5). Helically cut strips of abdominal aorta (n = 6) were suspended in isolated tissue baths for measurement of isometric force. Relaxation to acetylcholine (5.5 × 10<sup>–7</sup> M) and ATP (10<sup>–5</sup> M) was quantified in strips contracted with norepinephrine before and after exposure to indomethacin (14 µ M). In addition, the endothelium was damaged by exposing vessels to free radicals generated by electrolysis of the buffer (4 Hz, 9 V, 1 ms, 5 min). Following electrolysis of the buffer, relaxation responses to acetylcholine and ATP were significantly attenuated in both preparations. In the perfused heart, endothelium-dependent dilatation to acetylcholine, but not ATP were significantly inhibited in the presence of indomethacin or ibuprofen. In contrast, acetylcholine- and ATP-induced relaxation responses in the aorta were not altered by indomethacin. We conclude that prostaglandins contribute to acetylcholine-induced dilatation in the coronary bed but not in the abdominal aorta of the guinea pig. Furthermore, in the coronary bed, different endothelial factors mediate relaxation to acetylcholine and ATP.

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          Author and article information

          J Vasc Res
          Journal of Vascular Research
          S. Karger AG
          23 September 2008
          : 27
          : 6
          : 341-351
          Department of Physiology, University of Michigan Medical School, Ann Arbor, Mich., USA
          158828 Blood Vessels 1990;27:341–351
          © 1990 S. Karger AG, Basel

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          Page count
          Pages: 11
          Research Paper


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