Abstract
Activation of noradrenergic afferents arising from the A1 cell group of the caudal VLM excites neurosecretory AVP cells of both the supraoptic and paraventricular nuclei, thus stimulating the release of this potent vasoconstrictor into the circulation. Although this effect is mimicked by application of alpha 1-adrenoreceptor agonists to AVP cells, the excitatory effects of A1 afferents may not be mediated by activation of post-synaptic alpha 1-receptors. Evidence has also been obtained that the actions of A1 afferents are not dependent upon the release of excitatory amino acids or NPY, although the latter is co-stored with NA in A1 cells and potentiates the actions of low concentrations of NA on AVP cells. Although a projection to AVP and OXY neurosecretory cells from the A2 NA cell group of the NTS has been established, this projection does not appear to contribute directly to the control of SON AVP cell activity. Rather, NTS stimulation excites SON AVP cells via a relay projection through the A1 cell group. This pathway is likely to correspond to that involved in the stimulatory effects of haemorrhage and caval constriction on AVP secretion, although it is uncertain whether the effects of these particular stimuli are contingent upon unloading of arterial baroreceptors and atrial stretch receptors, as commonly presumed, or upon the activation of other receptors such as ventricular mechanoreceptors or chemoreceptors. On balance, current evidence suggests that the A1 projection is unlikely to be critically involved in mediating the effects of arterial baroreceptor, arterial chemoreceptor, or atrial stretch receptor activation on AVP cells.
Published Version
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