Cited by 129Neuropeptides and Animal PhysiologyAdrenal Hormones and DisordersStress Responses and Cortisol

The Role of Adrenal Nerves in the Regulation of Adrenocortical Functionsa

HOLZWARTH, M. A., CUNNINGHAM, L. A., KLEITMAN, N.·1987·Annals of the New York Academy of Sciences

Abstract

There is now convincing evidence for the distribution of several nerve plexuses in the outer zone of the adrenal cortex. At the ultrastructural level, the close proximity of nerve boutons to cortical cells establishes the anatomical substrate for a direct neural effect on adrenal cortical cell functions. Of those neurotransmitters and neuropeptides identified to date, catecholamine, VIP, and NPY appear to be most prevalent. Importantly, the amounts of morphologically identifiable catecholamine, VIP and NPY are differentially sensitive to alteration of several physiological conditions. Furthermore, the VIP plexus appears to be intrinsic to the adrenal while the catecholamine and NPY nerve fibers enter the adrenal along blood vessels. Together, these results suggest that these multiple nerve plexuses might exert control on several adrenocortical cellular processes in addition to the regulation of adrenal blood flow. Compensatory adrenal growth, a rapid proliferative response to unilateral adrenalectomy, was previously shown to be neurally mediated. The role of the catecholamine innervation in the mediation of this process has now been demonstrated. The elimination of the sympathetic nervous system by neonatal sympathectomy inhibited the proliferative response as measured by DNA synthesis. In vivo administration of beta-adrenergic receptor blockers did not inhibit the compensatory growth response. Furthermore, the beta-adrenergic agonist isoproterenol, inhibited the rate of DNA synthesis both in vivo and in vitro. The direct action of the beta-adrenergic agonist on the adrenocortical cell DNA synthesis rate suggests that the catecholaminergic nerves tonically inhibit cell proliferation associated with compensatory growth and that the release from the beta-adrenergic inhibition is necessary for compensatory growth. Whether inhibition of the beta-adrenergic innervation is the trigger for compensatory growth or whether it is permissive to the action of a still unidentified mitogenic substance, is not yet known. The direct role of VIP and catecholamines in the regulation of steroidogenesis has been investigated in vitro using the perifused capsule-glomerulosa preparation which is representative of a normal outer zone of the adrenal and is the site of the neural plexuses and identified receptors. Both VIP and isoproterenol stimulate steroidogenesis and specifically cause a greater increase in secretion of aldosterone than corticosterone. Although the concentrations of VIP and isoproterenol required to stimulate steroidogenesis are greater than reported circulating levels, release from resident nerves could provide high local concentrations.(ABSTRACT TRUNCATED AT 400 WORDS)

Integrity signals

Registry

Crossref · 10.1111/j.1749-6632.1987.tb24980.x

Cites

26 of 26 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • There is a neural SCN-adrenal gland connection via the autonomic nervous system, independent from HPA axis activation, that can transmit light information to the adrenal glands and modulate corticosterone release without changes in ACTH secretion.

    “significant evidence now points to a neural SCN-adrenal gland connection, via the autonomic nervous system and independent from the HPA axis activation [19, 20]: this multisynaptic pathway from the SCN to the adrenal gland is able to transmit light information to the adrenal glands, modulating corticosterone release without changes in ACTH secretion [21].”

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
HOLZWARTH, M. A., CUNNINGHAM, L. A., & KLEITMAN, N.
Affiliations
University of Illinois Urbana-Champaign (US)
Corresponding author
KLEITMAN, N.
Venue
Annals of the New York Academy of Sciences
Publisher
Wiley
Published
1987-12
Volume
512
Issue
1
Pages
449-464
ISSN
  • 0077-8923 (ISSN-L)
  • 1749-6632
OpenAlex
W1977107439
Cited by
129
References
26
Citations by year
2024: 1 · 2023: 1 · 2022: 2 · 2019: 2 · 2017: 2 · 2016: 1 · 2014: 2 · 2012: 2
FWCI
1.09
Type
journal article
Language
en
Open access
closed
Locations
  • Annals of the New York Academy of Sciences (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • School of Medicine, Emory University
  • National Institute of General Medical Sciences (5T32GM07)
  • National Center for Research Resources (S-O7RR7030)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
Keywords
adrenocortical function, catecholamine innervation, vasoactive intestinal peptide, neuropeptide Y, steroidogenesis, aldosterone secretion, adrenalectomy, beta-adrenergic receptors, isoproterenol, adrenal blood flow, zona glomerulosa, adrenal innervation, DNA synthesis
MeSH terms
Adrenal Cortex, Adrenalectomy, Aldosterone, Animals, Animals, Newborn, Autonomic Nervous System, Cell Division, Corticosterone, DNA Replication, Guanethidine, Hydroxydopamines, Kinetics, Male, Rats, Inbred Strains, Sympathectomy, Chemical, Oxidopamine, Rats, In Vitro Techniques

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review