Alterations in plasma noradrenaline in response to reflex modulation of sympathetic vasoconstrictor tone to skeletal muscles.

In man, stimulation and deactivation of carotid baroreceptors are accompanied by sympathetically-induced reduction and increase in total peripheral resistance, but not by alterations in plasma noradrenaline. This has been explained by the inability of arterial baroreflexes to sustainedly modulate sympathetic tone to skeletal muscle vessels on which plasma noradrenaline has been assumed largely to depend. In the present study nine subjects were submitted to procedures that cause a sustained alteration in muscle sympathetic vasoconstrictor tone, i.e. deactivation and stimulation of cardiopulmonary receptors. Cardiopulmonary receptor deactivation was achieved by a 20-min reduction in central venous pressure via application of subatmospheric pressure to the lower body, and the cardiopulmonary receptor stimulation by a 20-min increase in central venous pressure via passive leg raising. Plasma noradrenaline was measured radioenzymatically on blood sampled from an antecubital vein or the right atrium before, and at the 2nd, 5th, 10th and 20th min of each manoeuvre. The noradrenaline measurements were coupled with measurements of arterial blood pressure, heart rate and forearm blood flow and resistance (plethysmographic method). During reduction and increase in central venous pressure, blood pressure and heart rate did not change, whereas forearm vascular resistance markedly rose and fell with a peak response at 5 min and a subsequent plateau. These changes were accompanied by a marked rise and fall in plasma noradrenaline which also peaked within 5 min and were then sustained. Changes in forearm vascular resistance and noradrenaline showed a close qualitative parallelism, each increase in the former being accompanied by an increase in the latter, and vice-versa.(ABSTRACT TRUNCATED AT 250 WORDS)