High concentrations of catecholamines in human hypothalamic-hypophysial blood.

Abstract

While the hypothalamic-hypophysial portal system has been extensively studied in laboratory animals, equivalent studies have not been performed in humans. Here, we present an experimental procedure for collecting suprapituitary blood in man. To solve the question on the origin of such blood we investigated specific markers of hypothalamic secretory activity: the catecholamines (CAs). We found (a) norepinephrine (NE), dopamine (DA), and epinephrine (E) concentrations from 1.5 to 2.5, 3.5 to 4.5, and 6-to 10-fold higher, respectively, in suprapituitary than peripheral blood, (b) different NE/DA and NE/E ratios in favor of DA and E in suprapituitary blood, and (c), a complete (100%) group separation (suprapituitary vs. peripheral) when discriminant analysis included only DA and E. These data indicate that suprapituitary blood composition is different from that of the peripheral blood, and is particularly rich in CAs and claimed differences between DA and E release on one hand and NE release on the other in suprapituitary blood also are observed. We advance the hypothesis of a hypothalamic source of such amines draining via median eminence into portal vasculature, and name this blood "hypothalamic-hypophysial blood." Besides serving as "classical" neurotransmitters, CAs may also have a direct neurohormonal role in the regulation of the human hypothalamic-hypophysial function.

Acromegaly

“…The current in vivo studies are necessarily limited to an indirect assessment of GHRH secretion by measuring plasma GH profiles, whereas the in vitro investigations study the final morphologic product of the disease, that is, the tumor, and cannot draw any conclusions about the preexisting neurohormonal milieu to which this tissue had been exposed. The final answer is likely to come from in vivo studies in patients with acromegaly that will utilize recently developed methods: direct sampling of the pituitary portal blood (Paradisi et al 1989) and the use of GHRH-receptor antagonists (Lumpkin et al 1989) analogously to the use of G&U-I antagonist in patients with FSH-producing tumors (Daneshdoost et al 1990).…”