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November 1986

Abnormal Regulation of Noradrenergic Function in Panic Disorders: Effects of Clonidine in Healthy Subjects and Patients With Agoraphobia and Panic Disorder

Author Affiliations

From the Clinical Neuroscience Research Unit, Abraham Ribicoff Research Facilities, Connecticut Mental Health Center, and the Department of Psychiatry, Yale University School of Medicine, New Haven.

Arch Gen Psychiatry. 1986;43(11):1042-1054. doi:10.1001/archpsyc.1986.01800110028005

• Clonidine hydrochloride, an α2-adrenergic receptor agonist that decreases noradrenergic function, was administered to 21 healthy subjects and 26 drug-free patients with agoraphobia and panic attacks. Clonidine produced significantly greater decreases in plasma MHPG levels and sitting and standing diastolic blood pressure and significantly smaller increases in growth hormone levels and self-rated drowsiness in the patients. These findings indicate that the regulation of noradrenergic activity is aberrant in some patients with panic disorder, since a previous study demonstrated that patients with panic disorder exhibit increased plasma MHPG levels, blood pressure, and behavioral responses to the α2-adrenergic receptor antagonist yohimbine. The increased dynamic range of noradrenergic activity observed as an increased sensitivity to both clonidine and yohimbine may reflect abnormalities in the regulatory inputs to noradrenergic neurons, or dysfunction in the α2-adrenergic receptor effector coupling mechanism or the intracellular effector system.

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