{'fraction_non_alphanumeric': 0.030780243378668574, 'fraction_numerical': 0.009305654974946313, 'mean_word_length': 6.203608247422681, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Effects of metabolic inhibitors on endothelium‐dependent and endothelium‐independent vasodilatation of rat and rabbit aorta

1 Basal release of endothelium‐derived relaxing factor (EDRF) rendered endothelium‐containing rings of rat aorta 4.7 fold less sensitive to the contractile actions of phenylephrine and depressed the maximum response when compared with endothelium‐denuded rings. The responsiveness and maximum response to phenylephrine was, however, similar in rings of rabbit aorta with or without endothelium. 2 Rotenone (1 nm‐0.1 μm), an inhibitor of oxidative phosphorylation, induced a profound, irreversible blockade of phenylephrine‐induced tone in endothelium‐containing and endothelium‐denuded rings of rat aorta, but induced only slight inhibition of tone in rings of rabbit aorta. 3 2‐Deoxy glucose (10 mm), an inhibitor of glycolysis, had no effect on phenylephrine‐induced contraction in endothelium‐denuded rings of rat aorta, but inhibited reversibly the endothelium‐dependent depression of contraction in endothelium containing rings. 2‐Deoxy glucose had no effect on phenylephrine‐induced contraction in rings of rabbit aorta with or without endothelium. 4 Rotenone (0.1 μm) inhibited acetylcholine‐induced, endothelium‐dependent relaxation of phenylephrine‐contracted rings or rat and rabbit aorta. In endothelium‐denuded rings of rat aorta, relaxation induced by glyceryl trinitrate of isoprenaline was also inhibited, but relaxation induced by 8‐bromo cyclic GMP or dibutyryl cyclic AMP was not. Relaxation induced by verapamil on KCl‐contracted, endothelium‐denuded rings of rat aorta was also unaffected. 5 2‐Deoxy glucose (10 mm) inhibited acetylcholine‐induced, endothelium‐dependent relaxation of phenylephrine‐contracted rings of rat and rabbit aorta. In endothelium‐denuded rings of rat aorta, relaxation induced by glyceryl trinitrate and by isoprenaline was also inhibited, but relaxation induced by 8‐bromo cyclic GMP or dibutyryl cyclic AMP was not. Relaxation induced by verapamil on KCl‐contracted, endothelium‐denuded rings of rat aorta was also unaffected. 6 These data suggest that in rabbit and in rat aorta, rotenone inhibits acetylcholine‐induced relaxation by inhibiting EDRF production, and by depressing smooth muscle sensitivity to EDRF, respectively. They further suggest that 2‐deoxy glucose inhibits acetylcholine‐induced relaxation in both tissues by depressing the sensitivity to EDRF, probably as a result of reduced synthesis of cyclic GMP. The additional possibility that 2‐deoxy glucose inhibits EDRF production warrants further investigation. 7 The blockade by 2‐deoxy glucose of the endothelium‐dependent depression of phenylephrine‐induced tone in rat aorta probably reflects blockade of the actions of spontaneously released EDRF.