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Catechol-O-methyltransferase and blood pressure in humans

Official URL:https://doi.org/10.1161/01.CIR.0000022844.50161.3B
PubMed:View item in PubMed
Creators Name:Jordan, J. and Lipp, A. and Tank, J. and Schroeder, C. and Stoffels, M. and Franke, G. and Diedrich, A. and Arnold, G. and Goldstein, D.S. and Sharma, A.M. and Luft, F.C.
Journal Title:Circulation
Journal Abbreviation:Circulation
Volume:106
Number:4
Page Range:460-465
Date:23 July 2002
Keywords:Baroflex, Autonomic Nervous System, Multiple System Atrophy, Shy-Drager Syndrome, Adrenergic Receptors
Abstract:BACKGROUND: Whether catechol-O-methyltransferase (COMT), the enzyme that metabolizes extraneuronal norepinephrine, contributes to blood pressure regulation in humans is unknown METHODS AND RESULTS: We studied incremental doses of the COMT inhibitor entacapone, the sympathetic stimulant yohimbine, and placebo in 7 patients with multiple system atrophy (Shy Drager syndrome). We selected these unique subjects because norepinephrine exerts an exaggerated increase in blood pressure in these patients. Autonomic regulation was characterized with intravenous phenylephrine, nitroprusside, and trimethaphan. Patients were extremely hypersensitive to phenylephrine and nitroprusside. Trimethaphan elicited a profound depressor response. Phenylephrine sensitivity increased only slightly during ganglionic blockade. Entacapone increased systolic blood pressure dose-dependently; however, the pressor response to yohimbine was approximately 3.5 times greater than the maximal response to entacapone. CONCLUSIONS: COMT inhibition elicits a moderate, dose-dependent pressor response in the setting of severely impaired baroreflex buffering. Patients with multiple system atrophy allow for the characterization of subtle manipulations of norepinephrine turnover and blood pressure regulation in small numbers of subjects.
ISSN:0009-7322
Publisher:American Heart Association (U.S.A.)
Item Type:Article

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