Abstract

Adipose tissue is reported to modulate contractility in vascular smooth muscle, via a postulated relaxing factor (ADRF) derived from adipocytes. We studied pig LAD coronary arteries with or without endothelium (+/−E) and/or fat (+/−F). +E preparations produced greater forces (P<0.05), whereas +F preparations reduced force for KCl, Histamine and U46619, but not for ACh. The effects of fat were concentration‐dependent for +E and greatest at submax [U46619]. A role for endothelin‐1 was tested with U46619, using an ET receptor antagonist, PD145065 (1 μM). The COX inhibition with indomethacin (1E‐5M) was used to test for potential ADRF's. There were no changes in force after PD145065. Relaxation to indomethacin was also similar in endothelial and de‐endothelialized LAD, suggesting eicosanoids are not involved. Indomethacin significantly relaxed all LAD, but there was marked decrease in relaxation by LAD with fat indicating a potential prostanoid nature for ADRF. Our data suggest the presence of both an endothelial constricting factor and an ADRF and interactions between adipose tissue and the endothelium. Supported by AHA 0655300B and NIH HL61974(RJP).

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