Forty-six college students provided saliva samples just after taking an examination, one hour and 45 minutes later, and several days later, at a period of rest. As compared with baseline levels, the power stress of an examination was associated with an increase in salivary immunoglobulin A (S-IgA), a measure of B-cell immune function, and with an increase in norepinephrine (NE) concentrations in the saliva. The increase in NE was greater for those for whom n power was greater than n affiliation rather than for those for whom the reverse was true. Greater increases in, and levels of, NE at the examination and after were associated with greater subsequent drops in S-IgA, which reached below baseline levels for those for whom n power was stronger. The examination stimulated adrenergic activity, which in the long run depressed immune function for those with a strong power motive who had been most aroused adrenergically by the examination.
When isolated superfused cat mesentric arterial rings were exposed to norepinephrine(NE) 10'-6 g/ml, force initially increased but subsequently declined despite continuedadministration of NE. Phasic contractions occurred in 48% of the vessels. Norepinephrine concentrations just above threshold induced tonic contractions without escape. When NE was administered after brief exposure of the arterial rings to low-calcium solutions, peak force development and escape were both reduced and phasic contractions were abolished. Escape did not occur in potassium-depolarized vessels. The peak response was increased and escape was reduced by substituting sodium in the Krebs solution by lithium and by substituting chloride with iodide or perchlorate. Substitution of chloride by isethionate reduced the peak NE resonse and abolished escape. Propanolol was without effect. It is suggested that escape from NE vasoconstriction in mesenteric arteries is due to fading of propagated activity.
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