Mar 15, 1980

Neural control of colonic cell proliferation

P J Tutton, D H Barkla


The mitotic rate in rat colonic crypts and in dimethylhydrazine-induced colonic carcinomas was measured using a stathmokinetic technique. In sympathectomized animals cell proliferation was retarded in the crypts but not in the tumors, whereas in animals treated with Metaraminol, a drug which releases norepinephrine from nerve terminals, crypt cell but not tumor cell proliferation was accelerated. Blockade of alpha-adrenoceptors also inhibited crypt cell proliferation. However, stimulation of beta-adrenoceptors inhibited and blockade of beta-adrenoceptors accelerated tumor cell proliferation without influencing crypt cell proliferation. Injection of either serotonin or histamine stimulated tumor but not crypt cell proliferation and blockade or serotonin receptors or histamine H2-receptors inhibited tumor cell proliferation. It is postulated that cell proliferation in the colonic crypts, like that in the jejunal crypts, is under both endocrine and autonomic neural control whereas colonic tumor cell division is subject to endocrine regulation alone.

Mentioned in this Paper

Histamine Measurement
Taenia Coli
Sympathetic Nervous System
Serotonin Measurement
Malignant Tumor of Colon
Nerve Endings

About this Paper

Related Feeds

Adrenergic Receptors: Trafficking

Adrenergic receptor trafficking is an active physiological process where adrenergic receptors are relocated from one region of the cell to another or from one type of cell to another. Discover the latest research on adrenergic receptor trafficking here.

Related Papers

Virchows Archiv. B, Cell Pathology Including Molecular Pathology
P J Tutton
Clinica Chimica Acta; International Journal of Clinical Chemistry
Arbab SikanderKaushal Kishor Prasad
International Journal of Developmental Neuroscience : the Official Journal of the International Society for Developmental Neuroscience
Kaoru MiyazakiMasaaki Narita
© 2020 Meta ULC. All rights reserved