Temporal Relationship Between Interstitial Fluid Accumulation and Changes in Gonadotropin Receptor Numbers and Steroidogenesis in the Rat Testis

Abstract

Male rats aged 30 days were injected with 20.2 IU human chorionic gonadotropin (hCG), and the temporal changes in testicular interstitial fluid (IF) levels, the in vitro binding of [¹²⁵I]-hCG, and the steroidogenic capacity of the testis were assessed in detail from 2 to 40 h after injection. To monitor the temporal changes in in vivo binding of the injected hCG (i.e., LH-receptor occupancy) and the hCG levels in plasma and IF, other rats were injected with 20 IU unlabeled + 0.2 IU [¹²⁵I]-labeled hCG. Levels of ¹²⁵I in testis, plasma and IF were measured at 2–40 h. The specificity of the observed changes in vivo was checked by comparing levels of ¹²⁵I in testis, plasma and IF from rats injected with either hCG + [¹²⁵I]-hCG or hCG + [¹²⁵I]-bovine serum albumin. Testicular-bound hCG in vivo increased linearly between 2 and 8 h after injection, plateaued from 8 to 16 h and then declined by 87% up to 40 h. Plasma and IF levels of hCG were high at 2–10 h and then decreased progressively, the rate of decline being slower in IF than in plasma so that the IF:plasma hCG ratio increased steadily between 8 and 40 h. Injection of hCG caused accumulation of IF between 6 and 12 h with levels returning to normal at 40 h. The accumulation of IF (containing high levels of hCG) coincided with a relative increase in testicular-bound hCG in relation to plasma hormone levels, a change which persisted over the period from 10 to 16 h after injection. These changes induced by hCG, preceded “down regulation” of LH receptors (16 h onwards) and a dramatic reduction (70%) in the steroidogenic capacity of the testis (20–40 h). It is concluded that the hCG-induced accumulation of IF precedes, and may contribute to, the negative effects of hCG on Leydig cell function by increasing the transport of hCG to the Leydig cells. It is also suggested that IF may play an important role in the normal transport of LH to the Leydig cells.