The role of adenosine in dilator responses induced in arterioles and venules of rat skeletal muscle by systemic hypoxia.

1. In experiments on anaesthetized rats, we have studied the role of adenosine in mediating responses induced in individual arterioles and venules of the spinotrapezius muscle by systemic hypoxia. 2. During systemic hypoxia induced by breathing 6% O2 for 3 min, some arterioles and venules dilated while others constricted. Topical application of the adenosine receptor antagonist, 8 phenyl‐theophylline (8‐PT), to the spinotrapezius had no effect on the constrictor responses but greatly reduced the dilator responses. The vessels nearest to the capillary bed‐terminal arterioles and collecting venules‐‐were most affected; their mean changes in diameter were reduced from 39 and 8% to 11 and ‐1.6% respectively. 3. In accord with these results, topical application of adenosine (2 x 10(‐7)‐2 x 10(‐3) M) produced graded dilation of all sections of the arterial and venous trees; the terminal arterioles and collecting venules were most responsive, being dilated at maximum by 31 and 15% respectively. The dilator responses induced in those vessels that constricted during hypoxia were fully comparable with those that dilated during hypoxia. 4. Histochemical analysis of the spinotrapezius revealed that oxidative fibres that most readily release adenosine, glycolytic and mixed fibres were all evenly distributed throughout the muscle. There is no reason to suppose that some vessels are preferentially influenced by oxidative fibres. 5. These results indicate that adenosine plays a major role in dilating both arterioles and venules of muscle during systemic hypoxia. But, they are consistent with the idea that the adenosine that is important is not released from muscle fibres, but synthesized by 5'‐nucleotidase localized to the blood vessels; its activity may decrease proximally along the vascular tree and may vary from one vessel to another depending on the local O2 tension.