Abstract
Stressful sympathetic stimulation by cold pressor test in patients with essential hypertension results in an exaggerated response of the already elevated plasma adrenaline, heart rate, blood pressure, and α-adrenoceptor-mediated vasoconstriction when compared with normotensive subjects. The stress-induced increase in adrenaline was correlated with the attendant increase in blood pressure. The stress-induced reduction in forearm flow was reversed during infusion of the postjunctional α<sub>1</sub>-adrenoceptor blocker prazosin. Therefore, enhanced responses to sympathetic stress, as reflected and perhaps caused by an exaggerated rise in plasma adrenaline, may contribute to an increased α<sub>1</sub>-adrenoceptor-mediated vasoconstriction in essential hypertension.
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