Acute stress increases venomotor tone in conscious rats.

This study tested the hypothesis that acute psychological stress causes venoconstriction. Male Sprague-Dawley rats were instrumented with indwelling catheters in a femoral artery and vein and a balloon-tipped catheter in the right atrium. Mean arterial pressure (MAP), venous pressure, heart rate (HR), and mean circulatory filling pressure (MCFP) were monitored in conscious rats. Air-jet stress was performed before and after treatment with saline, chlorisondamine, phentolamine, or prazosin. Air-jet stress caused MAP, HR, and MCFP to increase by 10 +/- 1 mmHg, 31 +/- 4 beats/min, and 0.95 +/- 0.09 mmHg, respectively. Treatment with either chlorisondamine or phentolamine was equally effective in abolishing the stress-induced increases in MAP, HR, and MCFP. Prazosin treatment abolished the pressor response to air-jet stress but did not significantly affect the HR and MCFP responses. In contrast, pretreatment with the alpha 2-receptor antagonist rauwolscine hydrochloride abolished both the MAP and MCFP responses to air-jet stress but did not affect the HR response. These findings indicate that venoconstriction is an important component of the cardiovascular response to acute psychological stress. Stress-induced venoconstriction appears to be mediated primarily via the alpha 2-receptor subtype.