1. In humans, mental stress elicits vasodilatation in the muscle vascular beds of the forearm that may be neurally mediated. We sought to determine the extent to which this vasodilatation is due to sympathetic withdrawal, active neurogenic vasodilatation, or β-adrenergically mediated vasodilatation. 2. We simultaneously measured forearm blood flow and muscle sympathetic nerve traffic to the forearm during mental stress in humans. In a second study, we measured forearm blood flow responses to mental stress after selective blockade of α-adrenergic neurotransmission in one forearm. In a final study, we measured forearm blood flow responses to mental stress after unilateral anaesthetic blockade of the stellate ganglion, alone or in combination with selective β-adrenergic receptor blockade of the forearm. 3. During mental stress, muscle sympathetic nerve activity decreased from 5113 ± 788 to 1509 ± 494 total integrated activity min-1 (P < 0.05) and forearm vascular resistance decreased from 96 ± 29 to 33 ± 7 mmHg (dl of tissue) min ml-1 (P < 0.05). Considerable vasodilatation was still elicited by mental stress after selective blockade of α-adrenergic neurotransmission. Vasodilatation also occurred during mental stress after stellate ganglion blockade. This dilatation was reduced by selective blockade of β-adrenergic receptors in the forearm. 4. Our results support a role for both sympathetic withdrawal and β-adrenergic vasodilatation as the major causes of the forearm vasodilatation during mental stress in humans.
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