The Role of the Sympathetic Nervous System on Cerebral Blood Flow Regulation

Date

2010-12-01

Authors

Purkayastha, Sushmita

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Abstract

Despite evidence of an abundance of sympathetic and parasympathetic nerve fibers innervations of the α-adrenergic receptors in animals, the contribution of the sympathetic nervous system in the regulation of the cerebral vasculature in humans remains controversial. Previous investigators state that catecholamines do not penetrate the blood brain barrier (BBB), however, the tight junctions of the endothelium of the brain‟s arterioles are leaky and subject to modulation. An investigation of healthy human subjects and neurologically impaired patients using the norepinephrine spillover technique identified the presence of functional α adrenergic receptors within the cerebral vasculature. Therefore, we propose that the more permeable BBB surrounding the arterioles of the cerebral circulation allows the α-adrenergic receptors access to circulating as well as locally released norepinephrine within the brain, especially during exercise. Furthermore, arterial baroreceptor control of the cerebral vasculature has not been confirmed. However, our laboratory has demonstrated that α-1 adrenergic receptor blockade during acute hypotension influences dynamic cerebral autoregulation (dCA) and baroreflex mediated changes in cerebral blood flow (CBF). Therefore, the purpose of the investigations in this dissertation was to: i) determine if pharmacologic activation and blockade of α-1 adrenergic receptors resulted in cerebral vasoconstriction and vasodilatation, respectively, during rest and dynamic exercise; and ii) investigate the role of arterial baroreflex control of SNA on CBF regulation during rest and dynamic exercise. Pulsatile stimulation of the carotid baroreflex (CBR) with neck pressure (NP) and neck suction (NS) was used to entrain the variability of the reflex changes of the cerebral hemodynamic. In the first investigation we demonstrated an increase in cerebrovascular tone with activation of α-1 adrenergic receptor agonist with phenylephrine and with dynamic exercise. However, blockade of α-1 adrenergic receptors abolished the increase in vascular tone and caused impairment in dynamic CA. In the second investigation we demonstrated an increase in variability of the CBF and cerebral tissue oxygenation with pulsatile NP and this variability was abolished with α-1 adrenergic receptor blockade with prazosin. These findings identify the functional role of the α-1 adrenergic receptors in establishing cerebral vascular tone and their effects on dynamic CA and beat-to-beat dynamic CBF regulation.

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