Cortisol rapidly increases baroreflex sensitivity of heart rate control, but does not affect cardiac modulation of startle

Cortisol, the final product of human HPA axis activation, rapidly modulates the cortical processing of afferent
signals originating from the cardiovascular system. While peripheral effects have been excluded, it remains unclear
whether this effect is mediated by cortical or subcortical (e.g. brainstem) CNS mechanisms. Cardiac modulation
of startle (CMS) has been proposed as a method to reflect cardio-afferent signals at subcortical (potentially
brainstem-) level. Using a single blind, randomized controlled design, the cortisol group (n = 16 volunteers) received
1 mg cortisol intravenously, while the control group (n = 16) received a placebo substance. The CMS
procedure involved the assessment of eye blink responses to acoustic startle stimuli elicited at six different latencies
to ECG-recorded R-waves (R + 0, 100, 200, 300, 400 and 500 ms). CMS was assessed at four measurement
points: baseline, -16 min, +0 min, and +16 min relative to substance application. Baroreflex sensitivity (BRS)
of heart rate (HR) control was measured non-invasively based on spontaneous beat-to-beat HR and systolic blood
pressure changes. In the cortisol group, salivary cortisol concentration increased after IV cortisol administration,
indicating effective distribution of the substance throughout the body. Furthermore, BRS increased in the cortisol
group after cortisol infusion. There was no effect of cortisol on the CMS effect, however. These results suggest
that low doses of cortisol do not affect baro-afferent signals, but central or efferent components of the arterial
baroreflex circuit presumably via rapid, non-genomic mechanisms.