To the best of our knowledge no previous studies have investigated the effect of suppressing the HPA axis response during an acute psychological stress on levels of sAA, heart rate, blood pressure and subjective stress. While the DEX group had cortisol levels at or below the detection threshold of the assay, both groups showed an increase in subjective stress ratings with a rise in response to the anticipation period, and the actual TSST, this result being in line with Hellhammer and Schubert, who also recorded subjective stress during the TSST. The peak level of subjective stress was close to peak levels in sAA, heart rate and blood pressure responses, suggesting that the subjective stress rating is more closely associated with the activity of the SNS system rather than the HPA. This is best demonstrated in the DEX group, which, in the absence of any HPA response showed a trend for higher subjective stress responses, in line with a higher heart rate. One possible explanation for this is the fact that the changes of the SNS are tangible, for example an increase in heart rate, while there are no known perceptible physiological changes related to a change in cortisol secretion. The analysis of sAA showed a significant effect of Time with a typical response, peaking 10-minutes after onset of the stressor, similar to the systolic and diastolic blood pressure analysis. In the absence of any group or group by time effect. When interpreting a nonsignificant result it is important to consider the power to find an effect in the study sample if it was SCH772984 indeed existing in the population. There are a number of possible explanations for this effect. For one, it may be due to the central hypocortisol state created by the DST. The lack of negative feedback in the paraventricular nucleus of the hypothalamus will likely result in a CRH surge. It has been shown that there is a CRH-induced sympathetic activation, resulting in increased heart rate, blood pressure and glucose. Morphologically, CRH-secreting neurons from the hypothalamus project to the hindbrain and vice-versa. Also, the HPA and SNS seem to activate one another in a feed forward mechanism, via the CRH and locus coeruleus/norepinephrine connection. Moreover, it has been shown that NE potentiates the release of CRH and application of CRH to the LC neurons increases its firing rate, further confirming the physiological link between the two systems. Therefore, the hypocortisolemic state of the brain may be the cause for the elevated heart rate via a CRH surge, and the PVN and LC connection. Unfortunately, in the absence of any CRH measures this explanation must remain speculatory. Additionally, heart rate is mediated through the balance of the SNS and parasympathetic nervous system. Therefore, a possible effect of Dexamethasone via the parasympathetic nervous system could also be hypothesized.” A second explanation for the elevated heart rate could be the direct effect of dexamethasone on peripheral tissue involved in cardiovascular regulation.