Sep 1, 1976

Adrenergic mechanisms and the adenyl cyclase system in atopic dermatitis

The Journal of Investigative Dermatology
C E ReedT P Lee

Abstract

Patients with atopic dermatitis have abnormal autonomic responses of the arterioles, pilomotor smooth muscle, and sweat glands. Their lesions have been reported to contain increased amounts of the neurohumors, acetylcholine and norepinephrine, as well as increased activity of acetylcholinesterase and catechol-O-methyltransferase. In vitro studies of epidermis show that beta adrenergic agonists fail to evoke the normal inhibition of mitosis of basal cells of patients with atopic dermatitis. Epidermis removed not only from the lesions, but also from normal-appearing skin, responded abnormally. The increase in intracellular levels of cAMP after exposure to catecholamines was similar in normal and atopic epidermis. Lymphocytes and PMN leukocytes isolated from patients with atopic dermatitis show both a decreased physiologic response (glycogenolysis and inhibition of lysosome enzyme release) and a decreased rise in intracellular levels of cAMP upon incubation with beta agonists, but a normal response to PGE1. Cortisol increases the response of lymphocyte adenyl cyclase to both agonists and, in the case of the patients with atopic disease, more than overcomes the depressed response to beta agonists. Because the leukocytes respond nor...Continue Reading

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Mentioned in this Paper

Lysosome Assembly Pathway
COMT gene
Dermatitis, Atopic
Inhibition of Mitosis
Lymphocytes as Percentage of Blood Leukocytes (Lab Test)
Depressed - Symptom
Phosphoric diester hydrolase
Protoplasm
Lymphoid Cells
Catecholamines Measurement

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