A B S T R A C T This paper is a cross-sectional study of spontaneous benign prostatic hyperplasia (BPH) in a single canine species. The effects of aging and hormonal changes on the growth, histology, and glandular secretory function of the canine prostate were studied in 42 male beagles ranging in age from 8 mo to 9 yr. The beagle prostate enlarges for at least 6 yr, whether normal or hyperplastic. In contrast, prostatic secretory function, determined by ejaculate volume and total ejaculate protein, declines markedly after 4 yr of age. These reciprocal growth and functional changes in the prostate are closely associated with a progressive increase in the incidence of BPH, which is already apparent in some dogs by age two. With age there is a modest decrease in serum androgen levels with no apparent change in serum 17,3-estradiol levels. This suggests that the growth and functional changes that are associated with the development of BPH and are initiated very early in life reflect an altered sensitivity of the prostate to serum androgens or a response to the relative decrease in the serum androgen to estrogen ratio.

Stereological methods were employed to determine volume and surface densities of cytoplasmic organelles in Leydig cells of hamster, rat, rabbit, dog, and guinea pig testes. Contralateral testes were perfused in vitro with maximally stimulating gonadotropin concentrations to determine the capacity of these testes to secrete testosterone. Significantly different amounts of testosterone were secreted by in vitro perfused testes of the five species when maximally stimulated with ovine LH. Significant differences also were seen in the volume and surface densities of smooth endoplasmic reticulum, mitochondria, rough endoplasmic reticulum, and lipids in Leydig cell cytoplasm of the five species. Most interestingly, linear positive correlations were seen between testosterone secretion and smooth endoplasmic reticulum volume (r = 0.99) and surface (r = 0.99) densities. Thus, virtually all of the differences in testosterone secretion by maximally stimulated testes of five species could be accounted for by between-species differences in the amount of Leydig cell smooth endoplasmic reticulum.

Testes from guinea pigs, rabbits, dogs, rats, and hamsters perfused in vitro with maximally stimulating concentrations of ovine LH released 9.76 +/- 2.05, 12.80 +/- 3.15, 28.94 +/- 3.01, 3.18 +/- 0.41, and 0.70 +/- 0.12 microgram testosterone (T)/h, respectively. Adjusting for differences in testicular weight did not eliminate significant (P less than 0.01) species variation in testicular capacity for T secretion in response to ovine LH. Similarly, correction for Leydig cell mass, as determined by morphometric analysis, still left significant (P less than 0.01) differences in the testosterone secretion rates in response to ovine LH for guinea pigs (262.5 +/- 38.6 micrograms T/g Leydig cell), rabbits (205.5 +/- 50.7 micrograms T/g Leydig cell), dogs (116.4 +/- 14.8 micrograms T/g Leydig cell), rats (83.55 +/- 21.80 micrograms T/g Leydig cell), and hamsters (18.24 +/- 3.55 micrograms T/g Leydig cell). The data suggest that significant between-species variation of T production in response to ovine LH is not due to quantitative differences in the mass of Leydig cells.

Hypophysectomy or sc implantation of testosterone-estradiol 17 beta (T-E) filled polydimethylsiloxane capsules for 5 days caused a dramatic reduction in testosterone secretion when testes subsequently were perfused in vitro. The diminution in testosterone-secreting capacity of testes from T-E treated rats was coupled closely with reductions in the membrane surface areas of Leydig cell cytoplasmic organelles, particularly those of the smooth endoplasmic reticulum. Simultaneous treatment of T-E implanted rats with LH (12 micrograms/day), but not with FSH, PRL, TSH, or GH, maintained both the Leydig-cell cytoplasmic membranes and the capacity of testes to secrete testosterone in vitro. Testosterone secretion by testes from hypophysectomized rats treated simultaneously with T-E plus LH was identical to that in control rats. Therefore, T-E did not inhibit directly the Leydig cell steroidogenic apparatus. Taken together these results suggest that one of the trophic effects of LH in the Leydig cell is to maintained the integrity of smooth endoplasmic reticulum and enzymes responsible for the conversion of pregnenolone to testosterone.

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