Nitric oxide released from endothelial cells has been bioassayed previously, though EDHF, which differs from nitric oxide, has only recently been convincingly bioassayed. These studies, however, were performed in large conduit arteries. We wished to investigate whether these compounds could be bioassayed in resistance arteries. Rat small mesenteric arteries were set up in a dual chamber pressure myograph at 60 mm Hg, perfused at 100 ul/min and their lumen diameters measured by video-microscopy. Values given are the mean ±SEM of 5-6 vessels. The arteries had a mean diameter, when unstimulated, of 275 ±11 jam. When constricted with phenylephrine, acetylcholine (ACh) induced a vasodilation which was insensitive to the nitric oxide synthase inhibitor L-NAME (100 fiM) or indomethacin but was abolished by L-NAME in combination with 25 mM external K+ but not tetrabutylammonium (1 mM). To study the nature of the transferable relaxing factor, two vessels were set up in tandem and the endothelium of the downstream vessel was removed and confirmed by lack of vasodilation to ACh (1 uM; contraction of 2 ±2%). When ACh was added to the upstream, endothelium-intact vessel, both this and the downstream, endothelium-denuded, vessel increased in diameter by 70 ±5 and 30 ±2% of the induced tone, respectively. This indicates that EDRF(s) can be bioassayed from resistance arteries and that the EDHF in this artery may be different to that of rabbit carotid artery which is sensitive to tetrabutylammonium (Dong, Waldron, Galipeau, Cole and Triggle. Brit. J. Pharma-col. in press).
|Number of pages||1|
|Journal||Proceedings of the Western Pharmacology Society|
|Publication status||Published - 1997|
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