In 13 anesthetized dogs with their vagi cut and their carotid sinuses kept at constant pressure, the gracilis artery, cranial tibial artery, and lateral saphenous vein of the left hind limb were isolated and perfused at constant flow. In the right hind limb, muscle afferents were stimulated by electrodes in the thigh muscles. At 5 Hz, aortic blood pressure decreased 45 ± 8 mm Hg; perfusion pressure decreased in the gracilis muscle and the paw (26 ± 6 mm Hg and 26 ± 5 mm Hg, respectively) and increased in the saphenous vein (13 ± 3 mm Hg). These effects were not prevented by paralysis of the stimulated muscles, beta-receptor blockade, or administration of atropine or antihistaminic drugs. At 40 Hz, aortic blood pressure increased 29 ± 8 mm Hg; perfusion pressure increased in the gracilis muscle and the paw (33 ± 5 mm Hg and 33 ± 3 mm Hg, respectively) and decreased in the saphenous vein (20 ± 2 mm Hg). These effects were prevented or reversed by paralysis of the stimulated muscles. Similar effects were obtained by central stimulation of the femoral nerve. Left sympathectomy or alpha-receptor blockade abolished the responses in the isolated vascular beds. Thus, muscle contraction is necessary only to activate the muscle afferents which cause constriction of resistance vessels in muscle and paw and dilation of cutaneous veins.
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Clément et al. (1974) studied this question.
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