The control center regulates the blood levels of many hormones. Among these is adrenaline, released by the adrenal medulla. The adrenal medulla often operates in concert with the sympathetic nervous system, and the two together are sometimes viewed as one system, the "sympatho-adrenal axis". Thus we might instinctively guess that sympathectomy could somehow affect adrenaline levels in the blood, even without an obvious direct connection. This guess would prove to be correct, as ETS has been shown to lower adrenaline levels in the blood (see Nakamura 2002, 2005).
Effects of ETS on Plasma Levels of Noradrenaline and Adrenaline at Baseline and at Submaximal Exercise.
*p<0.05 vs before ETS; **p<0.01 vs before ETS.
Noradrenaline is released by sympathetic nerve terminals, so it is not surprising that blood levels of this catecholamine are reduced. However, most adrenaline is released into the bloodstream by the adrenal medulla, which is not directly affected by ETS. However, the adrenal medulla is part of the sympatho-adrenal axis, under the control of the hypothalamus, as discussed earlier. Dr. Nakamura had reported back in 1998 that ETS increases the blood level of a peptide called "atrial natriuretic peptide". So in the 2002 exercise paper he theorizes as to how this might offer clues to the mysterious low adrenaline levels:
"The sympathetic ganglion is not a simple relay station but a site modulated by short inter-neurons and a variety of neurotransmitters and receptors. Therefore, [T2-T3] ETS might have modified the sympathetic regulation of adrenaline secretion from the adrenal medulla. [T2-T3] ETS increases the plasma level of atrial natriuretic peptide, which has widespread sympatholytic activity. [T2-T3] ETS might have influenced the amount of adrenaline secreted from the adrenal medulla via changes in humoral factors such as atrial natriuretic peptide."(Nakamura 2002)Nakamura subsequently conducted a study on atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), and concluded "The plasma concentrations of ANP and BNP increased after ETS, independent of hemodynamic changes, and apparently because of the release of the inhibitory effects of the cardiac sympathetic nerves on natriuretic peptide secretion." (Nakamura 2005)
In other words, normally, the SNS inhibits the production of these peptides, so ETS surgery logically would cause them to increase. In turn, the peptides normally inhibit adrenaline production, so the increase in peptides brought on by ETS would further inhibit adrenaline production. Whatever the mechanism, it is now empirically confirmed that ETS surgery lowers blood levels of adrenaline. This could certainly help explain the "lowered alertness" and "chronic fatigue" reported so prevalently in the oral histories. Lowered alertness is also directly reported in empirical literature,, as we shall see in the section on mental functioning.
Empirical Status: Confirmed.
