Functional innervation of the adrenal cortex by the splanchnic nerve

Secretion of steroid hormones by the adrenal cortex is required to maintain whole body homeostasis; that is the ability to maintain blood pressure and volume, carbohydrate, protein and fat metabolism and immune and nervous system function within normal limits is dependent on adrenocortical hormones. The premise of this report is that autonomic-endocrine interactions occurring in the adrenal cortex are required for normal control of steroid secretion. Under non-stress conditions when reduced steroid secretion is required, splanchnic neural activity appears to be inhibitory, whereas during stress conditions when elevated steroid secretion is necessary, neural activity is excitatory. The capacity for innervation to produce both inhibitory and excitatory effects suggests that neural input must be encoded differentially; encoding could be dependent on the neurotransmitter released or on the intra-adrenal target affected. Neural input could act directly at the adrenal cell to affect steroidogenesis or act indirectly by changing adrenal blood flow. An index of the role of innervation has been obtained by assessing adrenal corticosteroid secretion after splanchnicectomy, severing the thoracic splanchnic nerve which is the major source of innervation of the adrenal gland. This approach has resulted in alterations in corticosteroid secretion under nonstress and stress conditions, but in many cases has demonstrated no profound effect on in vivo steroidogenesis. It is likely that splanchnicectomy results in variable secretory responses in part due to the multiplicity of adrenal neurotransmitter systems that are regulated by the splanchnic nerve. Splanchnicectomy alters multiple neurotransmitters at different adrenal sites. Splanchnic innervation acts as an extra-ACTH mechanism in the control of adrenal corticosteroid secretion, yet further elucidation of the physiological conditions under which splanchnic neural activity affects function is clearly warranted.