In the biopsychosocial model of challenge and threat by Blascovich and colleagues, the motivational states of challenge and threat that can arise in the context of motivated performance situations are distinguished on the basis of their different cardiovascular pattern:  challenge is marked by higher cardiac output (CO) and lower total peripheral resistance (TPR) than threat. In the "classical" literature adopting this model the explanation for this different cardiovascular pattern is the following (e.g., Seery, Neuroscience and Biobehavioral Reviews, 2011):"During threat, sympathetic-adrenomedullary activation is thought to be tempered by increased pituitary-adrenocortical activation. This is believed to inhibit the release of epinephrine and its vasodilatory effects, thereby resulting in relatively higher TPR and lower CO than challenge". This view has been the same over the last 30 years and does not seem to be really substantiated by empirical evidence (the only reference cited in this context is always the 1989 paper by Dienstbier). Surprisingly, to the best of my knowledge, no study in the challenge/threat literature has ever assessed these cardiovascular parameters and cortisol together to at least provide correlational support to this explanation.

Now, several studies have observed these different cardiovascular patterns to emerge quickly after challenge/threat manipulation, e.g. before a social-evaluative task. However, cortisol "takes time to react". Thus, it seems to me unlikely that cortisol can explain the different cardiovascular patterns of challenge and threat that emerge within seconds/minutes. Moreover, to the best of my knowledge, cortisol stimulates rather than inhibits the production of the catecholamines.

One factor that I thought could rather explain the "quick" differentiation between vasoconstriction/dilation is the degree of sympathetic-adrenomedullary activation: the degree of vasoconstriction/dilation depends on the level of circulating epinephrine with relatively higher levels causing vasoconstriction (alpha-adrenoceptor stimulation dominates) and relatively lower levels causing vasodilation (beta-adrenoceptor stimulation dominates).

Any comments that could shed some light on this issue are most welcome!