Objective: The coronary microvenous system may be determinant of ventricular distensibility and of resistance to coronary flow under conditions of arteriolar dilatation. Because responses of venules have not been well defined, in vitro responses of porcine venules and arterioles to neurohumoral substances were examined.
Methods: Porcine subepicardial venules (125-250 microns in diameter) and arterioles (100-200 microns in diameter) were studied in a pressurised no flow state with video microscopical imaging and electronic dimension analysis. After precontraction of vessels with the thromboxane A2 analogue U46619, agents were applied extraluminally.
Results: Responses of precontracted venules to sodium nitroprusside, adenosine, and adenosine 5' diphosphate (ADP) were comparable with those of similarly sized arterioles. By contrast, precontracted venules responded minimally to noradrenaline, whereas arterioles were dilated potently by this agent. Precontracted arterioles were dilated minimally by serotonin and were contracted slightly by acetylcholine, whereas venules dilated in response to either serotonin or acetylcholine. Serotonin and acetylcholine both produced greater contraction in non-precontracted arterioles than in non-precontracted venules. Responses of venules to most substances were minimally affected by changes in oxygen tension except when this was very low. Relaxation of venules by ADP, serotonin, and acetylcholine were all inhibited to varying degrees by indomethacin, methylene blue, and NG-methyl-L-arginine (L-NMMA). Both methylene blue and L-NMMA produced minimal but significant contraction of non-precontracted venules, indicating a small amount of basal release of endothelium derived relaxing factor.
Conclusion: Responses of coronary venules to acetylcholine, serotonin, and noradrenaline are opposite or of a significantly different magnitude when compared with the respective arteriolar responses. Relaxation of venules to ADP, serotonin, and acetylcholine is likely mediated at least in part by the release of endothelium derived relaxing factor and prostaglandins.