Objective: To determine the effects of local cooling on alpha-adrenergic responses in the fingers of patients with idiopathic Raynaud's disease.
Methods: Clonidine HCl and phenylephrine HCl were administered through a brachial artery catheter while blood flow was measured by plethysmography in cooled and uncooled fingers.
Results: Cooling potentiated alpha 2-adrenergic vasoconstriction in the patients but depressed this response in the controls.
Previous work in the canine saphenous vein has shown that cooling augments alpha 2- but not alpha 1-mediated contractile responses and that warming produces the opposite effects. Here we sought to determine whether these results occur in the human finger, a cutaneous vascular bed. Healthy men received brachial artery infusions of phenylephrine and clonidine with and without yohimbine while sympathetic tone was reduced by hearing the legs.
View Article and Find Full Text PDFPsychosom Med
November 1991
We have previously demonstrated that the vasospastic attacks of Raynaud's disease can be induced despite blockade of efferent digital nerves and that feedback-induced vasodilation is mediated through a non-neural, beta-adrenergic mechanism. Here, we sought to determine the role of sympathetic activity, as measured by plasma epinephrine and norepinephrine, during finger temperature feedback and autogenic training. Thirty-one female patients with idiopathic Raynaud's disease were randomly assigned to receive finger temperature feedback or autogenic training over 28 days.
View Article and Find Full Text PDFAlthough agonist-induced desensitization of adrenergic receptors has been previously demonstrated, the regulation of adrenergic receptors during acute psychological stress has not been investigated in humans. We studied 30 first year medical students during final examination week and one month earlier. Platelet alpha 2 receptor binding was measured using 3H-yohimbine and leukocyte beta 2 receptor binding was measured with 125I-CYP (Iodocyanopindolol).
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