Pituitary and gonadal response to exogenous LH-releasing hormone in the male domestic cat

To determine the influence of exogenous LH-releasing hormone (LHRH) on serum LH and testosterone, ten adult male domestic cats received three treatments on a rotating schedule at 10-day intervals as follows: (I) 0·1 ml saline i.m. (control); (II) 10 μg LHRH i.m., single injection; (III) 10 μg LHRH i.m., two injections given at a 2-h interval. Serial blood samples collected over a 360-min interval were analysed by radioimmunoassay for LH and testosterone. Although baseline serum LH values in saline-treated animals (treatment I) varied markedly among individual cats (2·2–29·2 μg/l), there was no evidence of pulsatile LH release or alterations in testosterone over time within individual males. In treatment II, the single injection of LHRH induced a rapid rise in mean serum LH within 30 min in all cats (mean peak, 88·2 ±9·8 μg/l), which returned to baseline by 120 min after LHRH. Mean testosterone increased within 30 min in this group (from 6·03 ±2·18 to 18·55 ±3·36 nmol/l), peaked at the 60-min collection (19·76 ± 2·77 nmol/l) and returned to baseline by the 150-min sample. After treatment III, serum LH peaked at 131·6±13·6μg/l within 30 min of the initial LHRH injection. A second injection of LHRH produced another LH surge within 30 min, but in all cats this second response was of a lower magnitude (mean peak, 69·0±14·5μg/l) and shorter duration (P<0·05). The second LHRH injection sustained peripheral testosterone levels for approximately 1 additional h. The increase in testosterone response was negatively correlated with pretreatment serum testosterone concentrations in both treatment groups (treatment II, r = −0·46; treatment III, r = −0·72). These results which provide an endocrinological data base for the male domestic cat: (1) demonstrate the acute sensitivity of the male pituitary-gonadal axis to a single injection of LHRH; (2) indicate that an additional LHRH challenge within 2 h results in a more attenuated LH surge, suggesting pituitary refractoriness to repeated LHRH administration; (3) suggest that gonadal sensitivity to LHRH administration is influenced by circulating testosterone. J. Endocr. (1985) 105, 175–181