The role of skin and muscle resistance vessels in reflexes mediated by the baroreceptor system

The role of skin and muscle vascular beds in baroreceptor-mediated alterations of peripheral vascular resistance was evaluated in six normal subjects in whom the skin circulation in one forearm was temporarily suppressed by epinephrine iontophoresis. Baroreceptor activity was enhanced by application of negative pressure to the neck (neck suction) and inhibited by application of lower body negative pressure. Forearm blood flow was measured simultaneously in both arms with strain gauge plethysmographs. Since blood flow in the treated arm consisted entirely of muscle flow, skin flow was calculated from the difference between total forearm flow in the intact arm and muscle flow in the treated arm. Vascular resistances were calculated as the ratio of mean arterial pressure to the blood flow of each vascular bed. During neck suction, mean arterial pressure decreased from an average of 89 to 75 mm of Hg (P < 0.005), heart rate decreased from an average of 60 to 55 beats/min (P < 0.005), and total skin and muscle flows remained essentially unchanged. Cutaneous vascular resistance decreased from an average of 75 to 49 mm of Hg/ml per 100 g per min (P < 0.05), muscle vascular resistance from 68 to 51 (P < 0.005), and total forearm vascular resistance from 36 to 24 (P < 0.025). During lower body negative pressure, heart rate increased from an average of 59 to 69 beats/min (P < 0.005), mean arterial pressure did not change significantly, and significant decreases occurred in forearm blood flow from 5.4 to 2.7 ml/100 g per min, in skin blood flow from 3.1 to 1.4, and in muscle blood flow from 2.3 to 1.3. Cutaneous vascular resistance increased from an average of 47 to 110 mm of Hg/ml per 100 g per min (P < 0.05), muscle vascular resistance from 43 to 72 (P < 0.005), and total forearm vascular resistance from 20 to 38 (P < 0.001). These results demonstrate that both the skin and muscle resistance vessels participate in reflex changes initiated by alterations in baroreceptor activity.

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