Prolactin Inhibits Carbachol-Dependent Secretion by Lacrimal Acinar Cells in Vitro

Abstract

Keratoconjunctivitis sicca, or dry eye, is characterized by decreased lacrimal fluid secretion. Since this disease is more prevalent in females than males, it has generally been assumed that the sex hormones are involved in its etiology. The sex steroids and the sexually dimorphic peptide hormone prolactin have been under investigation. There have been several reports that reveal a negative correlation between high levels of prolactin and lacrimal gland function. Studies with hypophysectomized rats¹ and with human subjects suggest that excessive levels of circulating prolactin (PRL) impair lacrimal secretion.² Prolactin levels are higher in females than males and rise during pregnancy, in accord with decreased lacrimal function (Schechter et al., unpublished data). Prolactin also seems to be closely linked to autoimmune diseases such as Sjögren’s Syndrome. Big prolactin, 60kD, is found to be overexpressed in salivary glandular epithelial cells of Sjögren’s syndrome patients,³ and hyperprolactinemia is found in 46% of patients with primary Sjögren’s syndrome.⁴ In addition, both prolactin and prolactin receptors are synthesized in the lacrimal gland,⁵ and PRL has been detected in human tears,⁶ suggesting that prolactin plays endocrine, paracrine, and autocrine roles in lacrimal gland function and maintenance of the ocular surface.