Clément, Denis

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.

The effect of stimulation of somatic afferents from muscle was investigated in 24 anesthetized dogs. The carotid sinuses were isolated and kept at constant pressure, the vagi were cut, and the left iliac artery was isolated and perfused at constant flow. Muscle afferents were stimulated by either inserting electrodes into the muscles of the right thigh or stimulating the central end of the right femoral nerve. Muscle stimulation at 5 Hz decreased perfusion pressure in the iliac artery 76 ± 6 mm Hg (mean ± SE ); the decrease was not prevented by paralysis of the stimulated muscles, administration of atropine or antihistamines, or -receptor blockade. Muscle stimulation at 40 Hz increased perfusion pressure in the iliac artery 28 ± 3 mm Hg. This increase was prevented or changed to a depressor response by muscle paralysis. Similar effects were obtained with femoral nerve stimulation. Both depressor and pressor responses persisted after the leg had been skinned and the muscles had been separated from their tendons, but they were abolished by left sympathectomy. Thus, skeletal muscle contraction is necessary for activation of the muscle afferents which cause reflex vasoconstriction but not for activation of those which cause reflex vasodilatation.

Pressure-dependent changes in afferent activity in the aortic and the sinus nerves were studied in 17 anesthetized dogs that were artificially ventilated with oxygen. Systemic arterial blood pressure was varied either continuously or in steps over the range of mean aortic blood pressure from 220 to 50 mm Hg with a pressurized reservoir connected to the abdominal aorta. Multifiber preparations from 20 aortic and 8 sinus nerves were used, and stimulusresponse curves were defined by measuring the mean impulse frequency at the various levels of pressure. Heart rate and pulse pressure were similar during recordings from both nerves. The two curves were S-shaped, with that for the aortic nerve being to the right of that for the sinus nerve. The change in activity was approximately linear from 200 to 120 mm Hg (mean aortic blood pressure) in the aortic nerve and from 180 to 80 mm Hg in the sinus nerve; there was no significant change in impulse frequency below mean blood pressures of 100 and 70 mm Hg, respectively. The threshold systolic blood pressure was 95 ± 3 (SE) mm Hg for the aortic receptors and 62 ± 4 mm Hg for the carotid sinus receptors. Thus, in the dog, the aortic baroreceptors are involved mainly in the control of high blood pressure, whereas at lower pressures the major control occurs through the carotid sinus baroreflex.