Effects of naloxone and thyrotropin-releasing hormone on plasma catecholamines, corticosterone, and arterial pressure in normal and endotoxemic rats.

To investigate the possible involvement of the adrenal cortex and medulla in the cardiovascular effects of naloxone and thyrotropin-releasing hormone (TRH) in endotoxic shock, plasma epinephrine, norepinephrine, dopamine, and corticosterone were measured along with hemodynamic variables during naloxone and TRH treatment of normal and endotoxemic rats. In the absence of endotoxemia, naloxone (3 mg/kg, iv) did not significantly alter mean arterial pressure or plasma catecholamine or corticosterone levels. In contrast, following TRH administration (4 mg/kg, iv), an increase in mean arterial pressure was associated with significant increases in plasma epinephrine, norepinephrine, and corticosterone. TRH also produced a transient increase in plasma glucose levels. Endotoxic shock was associated with marked increases in plasma catecholamine levels, with epinephrine levels showing the greatest change, and significant though less pronounced increases in corticosterone. Both naloxone and TRH significantly elevated mean arterial pressures of endotoxemic rats, although neither of these compounds significantly altered the plasma catecholamine and corticosterone responses to endotoxin. Naloxone and TRH also failed to alter endotoxin-induced changes in plasma glucose levels. These results indicate that the cardiovascular effects of naloxone and TRH in endotoxic shock do not simply arise from an enhancement of adrenal catecholamine or corticosterone secretion.