Pelletier, C

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.

The vascular effects of graded stimulation of the carotid chemoreceptors were studied in 13 anesthetized and artificially ventilated dogs, and stimulus-response curves were defined. The carotid bifurcations were isolated and perfused at constant pressure, and the vagi were cut. Autologous blood collected in a reservoir was equilibrated at Po 2 varying from 104 to 34 mm Hg, Pco 2 from 39 to 81 mm Hg, and pH from 7.46 to 6.87 and was used to stimulate the carotid chemoreceptors. Systemic arterial Po 2 , Pco 2 , and pH were kept normal. Reflex increases in aortic blood pressure and in hind-limb perfusion pressure (constant-flow perfusion) were first seen with Po 2 of 70 mm Hg or Pco 2 > 39 mm Hg. The vascular responses increased linearly with lower Po 2 or higher Pco 2 , until tensions of 34 and 71 mm Hg, respectively, were reached. These stimuli caused a reflex dilatation of the perfused saphenous vein that was also proportional to the degree of stimulation. Increasing the pH of the blood perfusing the chemoreceptors decreased these changes by more than 50%; decreases in pH, with normal Po 2 and Pco 2 , caused marked vascular responses, indicating an important role of pH in the activation of the chemoreflex mechanism.

Experiments were conducted in 35 anesthetized dogs to study the circulatory adjustments, after hemorrhage, mediated by vagal afferents from the cardiopulmonary area. With the aortic baroreceptors and chemoreceptors denervated and carotid baroreceptor and chemoreceptor activity held constant, hemorrhage of 10% of blood volume caused an increase in heart rate and constriction of the resistance vessels of the hindlimb, renal, and mesenteric beds and of the splanchnic venous bed. Vagotomy abolished these responses to hemorrhage, resulting in a greater decrease in blood pressure. With the carotid baroreflex operative, the constriction of the renal and mesenteric resistance vessels and of the splanchnic venous bed were similar to that obtained with only the vagi operative, but the constriction of the hindlimb resistance vessels was much greater and aortic pressure was better maintained. It is concluded that receptors in the cardiopulmonary area, subserved by vagal afferents, exert their main influence on the splanchnic resistance and capacitance vessels and on the renal circulation, whereas the carotid baroreceptors predominantly affect the muscle vessels.