Previous studies have shown unequivocally a lack of pituitary-adrenocortical stress hormone activation during lactate-induced panic attacks despite considerable psychopathological alterations, signs of arousal and several vegetative symptoms regularly occurring during stressful conditions. To study the possible inhibitory action of atrial natriuretic hormone (ANH) on adrenocorticotrophic hormone (ACTH) and cortisol release in humans, 10 patients with panic disorder (DSM-III-R) received sodium lactate and placebo (0.9% saline) infusions and ten healthy comparison subjects additionally received a 2.5% saline infusion and the response of ANH, vasopressin, ACTH, cortisol, and several biochemical and physiological cardiovascular parameters were measured. In comparison to placebo, lactate infusion led to enhanced ANH levels in both non-panicking comparison subjects and panickers. Importantly, panickers showed significantly lower baseline levels of ANH than comparison subjects followed by a faster release. No significant concomitant changes in vasopressin, ACTH, and cortisol were observed. During lactate infusion, heart rate was accelerated considerably in the two groups; in contrast, the reduction of pCO2 indicated an enhanced ventilation only in panickers. The pattern of ANH release cannot be attributed simply to either the volume load administered, the cardiac activation or an osmotic effect since neither 0.9 nor 2.5% saline resulted in comparable effects. Additional central nervous mechanisms must be considered for the increased ANH concentrations in lactate-induced panic attacks. We propose that the release of ANH is an intrinsic mechanism contributing to the apparent unresponsiveness of the pituitary-adrenocortical system in lactate-induced panic attacks. In addition, we surmise that ANH may also play a role in the yet unknown mechanisms for termination of panic attacks, e.g. either by inhibitory actions on the locus coeruleus or by bronchiorelaxation and consecutive decatastrophization.
