HCG BINDING TO THE TESTICULAR LH RECEPTOR IS SIMILAR IN FERTILE, SUBFERTILE, AND INFERTILE STALLIONS

Recent evidence in our laboratory suggests that the cause of idiopathi c subfertility/infertility in breeding stallions may originate in the testes at the luteinizing hormone (LH) receptor or postreceptor level. The objective of this research was to determine if LH receptor bindin g activity is altered in subfertile and infertile stallions. Six ferti le, three subfertile, and three infertile stallions, ages 11-23 years, were classified according to normal semen parameters and pregnancy ra tes and then castrated in the breeding season. Blood was collected pri or to castration, and plasma was stored until analyzed for LH, follicl e stimulating hormone (FSH), estrogen conjugates (EC), estradiol (E-2) , testosterone (T), and inhibin (I) by radioimmunoassay (RIA). Testicu lar cell membranes were prepared and snap-frozen until analyzed for LH binding activity by radioreceptorassay (RRA) using increasing amounts of I-125 human chorionic gonadotropin (hCG). Luteinizing hormone rece ptor numbers and affinity constants were determined by Scatchard analy sis. Plasma LH, FSH, EC, E-2, and T levels did not differ between fert ile and subfertile stallions, but LH and FSH were significantly higher (P < 0.05) and EC, E-2, T, and I levels were significantly lower (P < 0.05) in infertile stallions as compared to fertile and subfertile st allions. Receptor number (R-t and affinity constants K-a were similar (P > 0.05) between fertile (R-t = 9.44 x 10(-11) M, K-a = 0.300 x 10(1 0) M-1), subfertile (R-t = 13.02 x 10(-11) M, K-a = 0.194 x 10(10) M-1 ), and infertile (R-t = 7.65 x 10(-11) M, K-a = 0.380 x 10(10) M-1) st allions. In conclusion, these data suggest that an endocrine dysfuncti on in the testes of stallions with poor fertility may not be due to a LH receptor disorder but may be due to a postreceptor malfunction.