Forearm sympathetic withdrawal and vasodilatation during mental stress in humans

Abstract

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. 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. During mental stress, muscle sympathetic nerve activity decreased from 5113 ± 788 to 1509 ± 494 total integrated activity min− (P < 0.05) and forearm vascular resistance decreased from 96 ± 29 to 33 ± 7 mmHg (dl of tissue) min ml− (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. 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.

Cardiovascular and renal responses to mental challenge in highly and moderately active males with a family history of hypertension

“…These results suggest that the initial forearm vasodilatation response to stress and the reductions in forearm vascular resistance are reinforced by ␤2-adrenergic or cholinergic activity. Furthermore, Halliwell et al 25 examined skeletal muscle vasodilatation to mental stress in order to determine the extent to which this response was due to sympathetic withdrawal, active neurogenic vasodilatation, or ␤-adrenergically mediated vasodilatation. Firstly, they found that muscle sympathetic nerve activity to the forearm was inhibited during mental stress (a 2.5-min Stroop task), suggesting that sympathetic vasoconstrictor withdrawal may contribute to the vasodilatation response.…”

Sympathetic Vascular Tone in Human Obesity

“…Several mechanisms have been proposed. First, sympathetic withdrawal during mental stress could cause vasodilatation [Halliwill et al, 1997]. This possibility appears unlikely because mental stress has been associated with unaltered or increased mSNA.…”

“…The activation of β 2 -adrenergic receptors could contribute to the increased expression of endothelial nitric oxide [Dawes et al, 1997;]. Furthermore, increases in arterial pressure during mental stress could augment vascular shear stress, which also stimulates synthesis and release of nitric oxide by the vascular endothelium [Halliwill et al, 1997]. Importantly, forearm resistance vessel endothelial dysfunction has been observed in uncomplicated obesity [Perticone et al, 2000].…”

“…Alternatively, the sympatho-adrenal response to mental stress could be altered in obesity [Halliwill et al, 1997] but epinephrine was not measured during mental mathematical test to assess this possibility.…”

The effects of exercise on haemodynamic function in relation to the familial hypertension risk model

“…48 The skeletal muscle vasodilatation response to mental stress is thought to be mediated by both the withdrawal of sympathetic neural vasoconstrictor influences and vasodilatation by b-adrenergic pathways involving epinephrine. 49 Therefore, it is likely that the mechanisms for an attenuated postexercise vasodilatation response to stress in FH þ are linked to the sympathetic nervous system. Indeed previous studies in normal subjects have consistently demonstrated reductions in catecholamine reactivity to stress tasks (the difference in catecholamine concentration following stress compared with baseline) following an acute bout of exercise.…”