ACUTE STRESS INCREASES VENOMOTOR TONE IN CONSCIOUS RATS

This study tested the hypothesis that acute psychological stress cause s venoconstriction. Male Sprague-Dawley rats were instrumented with in dwelling catheters in a femoral artery and vein and a balloon-tipped c atheter in the right atrium. Mean arterial pressure (MAP), venous pres sure, heart rate (HR), and mean circulatory filling pressure (MCFP) we re monitored in conscious rats. Air-jet stress was performed before an d after treatment with saline, chlorisondamine, phentolamine, or prazo sin. Air-jet stress caused MAP, HR, and MCFP to increase by 10 +/- 1 m mHg, 31 +/- 4 beats/min, and 0.95 +/- 0.09 mmHg, respectively. Treatme nt with either chlorisondamine or phentolamine was equally effective i n abolishing the stress-induced increases in MAP, HR, and MCFP. Prazos in treatment abolished the presser response to air-jet stress but did not significantly affect the HR and MCFP responses. In contrast, pretr eatment with the alpha(2)-receptor antagonist rauwolscine hydrochlorid e abolished both the MAP and MCFP responses to air-jet stress but did not affect the HR response. These findings indicate that venoconstrict ion is an important component of the cardiovascular response to acute psychological stress. Stress-induced venoconstriction appears to be me diated primarily via the alpha(2)-receptor subtype.