Capillary adrenoceptors in rat skeletal muscle.

The purpose of this study was to examine whether functional alpha- and beta-adrenoceptors exist on capillaries of rat skeletal muscle, and further to determine which subtype of these receptors predominates on these capillaries. Using intravital video microscopy, we measured red blood cell velocity (VRBC) responses in capillaries of rat extensor digitorum longus muscle (EDL) following a local application of these agonists: norepinephrine (NE; alpha 1, alpha 2; 10(-7) to 3 x 10(-3) M), phenylephrine (PE; alpha 1; 3 x 10(-4) to 10(-2) M), clonidine (CLO; alpha 2; 3 x 10(-3) to 10(-2) M), UK14304 (alpha 2; 3 x 10(-4) to 10(-2) M), and isoproterenol (IPR; beta 1, beta 2; 10(-7) to 3 x 10(-3) M). Responses to NE (10(-5) M) were also measured after a local pretreatment with prazosin (alpha 1 antagonist; 10(-5) to 10(-3) M) and rauwolscine (alpha 2 antagonist; 3 x 10(-4) to 3 x 10(-2) M), while responses to IPR (10(-5) M) were measured after local atenolol (ATE; beta 1 antagonist; 10(-3) to 10(-2) M) and butoxamine (BUT; beta 2 antagonist; 10(-3) to 10(-2) M) pretreatment. The overall control VRBC was 226 microns/sec. NE, PE, CLO, and UK14304 resulted in concentration-dependent decreases of VRBC (from -12 to -89%) from the control level, while IPR caused concentration-dependent increases (17 to 174%). PE reduced VRBC to a larger degree than CLO and UK14304. NE-induced VRBC responses tended to be attenuated more by prazosin than by rauwolscine. Both ATE (10(-2) M) and BUT (10(-3) and 10(-2) M) alone decreased VRBC. However, only ATE significantly attenuated the IPR-induced VRBC responses. These results suggest that the capillary of rat EDL muscle has alpha- and beta-adrenoceptors. From the two alpha-adrenoceptor subtypes, the capillary may be predominated by the alpha 1-adrenoceptors.