The role of the autonomic nervous system in secretory
immunoglobulin A (sIgA) responses to laboratory challenge
was explored in a study in which sIgA and cardiovascular
activity were recorded at rest and during mental arithmetic
and paced breathing. These tasks were selected to preferentially
engage the sympathetic and parasympathetic nervous systems,
respectively. Mental arithmetic elicited a mixed pattern
of increased alpha- and beta-adrenergic activity and a
reduction in parasympathetic activity; diastolic blood
pressure, total peripheral resistance, and systolic blood
pressure increased, preejection period shortened, and heart
rate variability decreased. In contrast, paced breathing
primarily elicited an increase in parasympathetic activity;
heart rate variability increased. Mental arithmetic also
provoked an increase in sIgA concentration but no change
in saliva volume, whereas paced breathing affected neither
sIgA concentration nor saliva volume. These data suggest
that sIgA responses to laboratory challenges are mediated
by sympathetic rather than parasympathetic processes.

Patients with rheumatoid arthritis are at increased risk for myocardial infarction. It has been hypothesized that mental stress-induced cardiovascular reactions may play a role in the triggering of myocardial infarction. Cardiovascular activity was measured during rest, stress, and recovery in rheumatoid arthritis patients with high systemic inflammation (C-reactive protein>8mg/l), rheumatoid arthritis patients with low systemic inflammation (C-reactive protein≤8mg/l), and osteoarthritis patients. Systemic vascular resistance increased only in rheumatoid arthritis patients with high systemic inflammation. Heart rate and mean arterial pressure increased during the stress task in all groups. Thus, acute cardiovascular events in rheumatoid arthritis patients may be related to stress-induced increases in systemic vascular resistance, particularly in patients with high levels of systemic inflammation.

Objective
The idea that distinct psychosocial factors may underlie specific patterns of neuroendocrine stress responses has been a topic of recurrent debate. We examined a recent contribution to this debate, the Social Self Preservation Theory, which predicts that stressors involving social evaluative threat (SET) characteristically activate the hypothalamic-pituitary-adrenal (HPA) axis.

Methods
Sixty-one healthy university students (31 females) performed a challenging speech task in one of three conditions that aimed to impose increasing levels of SET: performing the task alone (no social evaluation), with 1 evaluating observer, or with 4 evaluating observers. Indices of sympathetic (pre-ejection period) and parasympathetic (heart rate variability) cardiac drive were obtained by impedance- and electrocardiography. Salivary cortisol was used to index HPA activity. Questionnaires assessed affective responses.

Results
Affective responses (shame/embarrassment, anxiety, negative affect, and self-esteem), cortisol, heart rate, sympathetic, and parasympathetic activation all differentiated evaluative from non-evaluative task conditions (p<.001). The largest effect-sizes were observed for cardiac autonomic responses. Physiological reactivity increased in parallel with increasing audience size (p<.001). A rise in cortisol was predicted by sympathetic activation during the task (p<.001), but not by affective responses. Conclusion It would appear that SET determines the magnitude, rather than the pattern, of physiological activation. This potential to broadly perturb multiple physiological systems may help explain why social stress has been associated with a range of health outcomes. We propose a threshold-activation model as a physiological explanation for why engaging stressors, such as those involving social evaluation or uncontrollability, may appear to selectively induce cortisol release.