Catecholamine Effects on Leydig Cell Steroidogenesis

Abstract

Luteinizing hormone (LH) is without question the most important regulator of Leydig cell steroidogenesis. In some species such as the ram there is concordance between episodes of LH secretion and episodes of testosterone secretion (Lincoln, 1976). In others, such as man and rat, the concordance is less precise. Ellis and Desjardins (1982) have, for example, suggested that two or more episodes of LH secretion must occur within 70 min of each other to induce an episode of testosterone secretion. LH not only acutely stimulates testosterone secretion but is important in maintaining the morphological and enzymatic attributes required for androgen production (Wing et al., 1984). There are, however, a number of situations where testosterone secretion appears to be altered without a corresponding change in LH secretion. Examples include “testitoxicosis”, which is characterized by precocious puberty in boys with low serum gonadotropin concentrations (Weirman et al., 1985); the “testicular hemicastration response” in rats where the testosterone secretion rate of the remaining testis doubles within 24 h of hemicastration without a corresponding increase in serum LH concentrations (Frankel and Wright, 1982); the decline in serum testosterone concentrations in fetal male rats and mice late in gestation despite increasing serum LH concentrations (Pointis et al., 1980; Slob et al., 1980; Habert and Picon, 1982); and the reduction in serum testosterone concentrations induced by stress which has variable effects on LH secretion (Aona et al., 1976; Du Ruisseau et al., 1978; Gray et al., 1978; Tache et al., 1980). It must be noted that the dynamic nature of LH secretion makes it difficult to prove that small alterations in LH secretion have not occurred in situations where testosterone secretion appears to vary independent of changes in LH concentrations. Possible alterations in testicular blood flow or androgen metabolism also complicate interpretation. However, LH-independent testosterone secretion raises the possibility that factors other than LH influence Leydig cell steroidogenesis. There is considerable evidence for direct effects of prolactin (Purvis et al., 1979), estrogens (Moger, 1980), vasopressin (Adashi et al., 1981, 1984) and, in some species, gonadotropin-releasing hormone (Sharpe, 1983) on Leydig cells and for indirect effects of follicle-stimulating hormone (FSH) acting on Leydig cells via an unidentified local testicular factor (Moger and Murphy, 1982). This review will focus on our recent studies that indicate that the catecholamines epinephrine and norepinephrine can directly stimulate Leydig cell steroidogenesis and thus may have physiologic or pathophysiologic roles in the LH-independent regulation of steroidogenesis.