Lack of effect of the alpha-adrenergic agonist clonidine on pulsatile luteinizing hormone secretion in a double blind study in men.

This study was designed to evaluate the effects of alpha-adrenergic stimulation on the hypothalamic LHRH pulse generator in men. In 10 normal men, venous blood was sampled on 2 occasions at 10-min intervals for 8 h, beginning 30 min after oral administration of either placebo or 0.3 mg clonidine according to a randomized double blind protocol. Compared to placebo, clonidine induced a marked release of GH (P less than 0.0001 for response areas under the curve after placebo and clonidine), a fall in systolic and diastolic blood pressure and in heart rate (P less than 0.002 for areas under the curve after placebo and clonidine), and feelings of sedation and dry mouth (P less than 0.002 and P less than 0.05 for areas under the cumulative scores for changes in alertness and salivation, respectively). There was no difference between the results obtained after placebo and clonidine for the mean number of LH pulses [3.3 +/- 0.4 (+/- SE) and 3.3 +/- 0.3 pulses/8 h], for the mean amplitude of all LH pulses (3.8 +/- 0.4 and 4.1 +/- 0.5 IU/L), or for the areas under the LH concentration-time curve (2741 +/- 251 and 2728 +/- 215 IU/L.min). The lack of effect of clonidine on LH secretion at a dose that effectively induced GH secretion and other centrally mediated effects indicates that the actions of testosterone and opiates to decelerate the frequency of the LHRH pulse generator in men are not mediated by diminished alpha-adrenergic stimulation. From these results, taken together with previous data, we conclude that alpha-adrenergic systems do not play a major role in the regulation of episodic LH release in men.