Abstract
1. Studies have been made in the anaesthetized rat of the roles played by alpha- and beta-adrenoreceptor stimulation in determining diameter changes induced in individual arterioles and venules of the spinotrapezius muscle during systemic hypoxia (breathing 6% O2 for 3 min). 2. Topical application to the spinotrapezius of phentolamine, the alpha-adrenoreceptor antagonist, or sotalol, the beta-adrenoreceptor antagonist, had no effect on the fall in systemic arterial pressure and tachycardia induced by hypoxia. 3. All arterioles and venules showed a decrease in diameter in response to topical application of noradrenaline (10(-6) g ml-1): these responses were abolished by topical application of phentolamine. Moreover, those arterioles and venules that showed a decrease in diameter during hypoxia before phentolamine, showed a significantly smaller decrease, or an increase in diameter after phentolamine. This effect was most marked in primary and secondary arterioles (13-50 microns diameter). 4. All arterioles and venules showed an increase in diameter in response to topical application of isoprenaline (10(-6) g ml-1); these responses were abolished by topical application of sotalol. Moreover, these arterioles and venules that showed an increase in diameter during hypoxia before sotalol, showed a significantly smaller increase or even a decrease in diameter after sotalol. 5. These results suggest that during hypoxia the arterioles of skeletal muscle, especially primary and secondary arterioles, are under the constrictor influence of a reflex increase in sympathetic nerve activity while the venules, which have no sympathetic innervation, are under the constrictor influence of circulating catecholamines. They also suggest that in individual arterioles and venules, these constrictor influences may be overcome by dilatation mediated by the beta-adrenoreceptor influence of circulating catecholamines. 6. Since some arterioles and venules still showed constriction during hypoxia after phentolamine and some still showed dilatation during hypoxia after sotalol, it seems that factors other than catecholamines contribute to the diameter changes. It is suggested that locally released metabolites exert a substantial dilator influence, particularly on terminal arterioles and collecting venules, those vessels nearest to the capillary bed.