Abstract
The administration of C, an α2 adrenergic agonist, induces GH secretion, sedation and hypotension. To test the hypothesis that these effects are independent of one another, we measured GH responses to oral C (4 μg/kg) in 14 SS patients whose post-exercise GH was <7 ng/ml and in 5 TS patients. Plasma C levels, blood pressure and degree of sedation were recorded as were plasma levels of 3-methoxy-4 hydroxyphenyl glycol (MHPG). To determine the persistence of GH responsiveness the 5 TS were restudied after 3 mos Rx with C. GH peaks (mean 17.4±3 ng/ml) occurred at 60-90 min. in all TS and 9/14 SS patients. There was no tendency for responsiveness to diminish after Rx with C with mean post Rx GH peaks of 22±5ng/ml in the 5 TS. In 5/14 SS, all GH deficient on insulin testing, peak GH was <3 ng/ml. C levels rose to a peak of 1.2±3ng/ml at 60′, preceding the GH peak by 30′. An observed 12% fall in MHPG levels (attributable to a C-mediated reduction in central nervous system (CNS) noradrenergic activity) was not related to the timing or extent of the GH peaks. These peaks also bore little temporal relationship to the slight hypotension or marked sedation occurring after oral C. We conclude that C is a highly effective tool for the diagnosis of GH deficiency and that the GH response to C is sustained during chronic Rx with C. Our data support animal studies which suggest that C exerts its various effects at multiple sites in the CNS.
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