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Journal of Clinical Endocrinology & Metabolism Vol. 67, No. 1 139-143
doi:10.1210/jcem-67-1-139
Copyright © 1988 by the Endocrine Society.
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Hemodynamic Reactivity to Sympathoadrenal Stimulation in Adrenalectomized Women*

J. W. M. LENDERS, J. H. M. PETERS, G. F. F. PIETERS, J. J. WILLEMSEN and Th. THIEN

Department of Internal Medicine, Division of General Internal Medicine, and Division of Endocrinology, Department of Experimental and Chemical Endocrinology, St. Radboud University Hospital Nijmegen, The Netherlands

Address all correspondence and requests for reprints to: J. W. M. Lenders, Department of Medicine, St. Radboud University Hospital, Geert Grooteplein Zuid 8, 6525 GA Nijmegen, The Netherlands.

To determine the extent to which circulating epinephrine (E) mediates the cardiovascular effects of sympathoadrenal stimulation, we studied the blood pressure (BP), heart rate, forearm vascular resistance, and plasma catecholamine responses to a mental arithmetic test, head-up tilt test, and cold pressor test in 10 adrenalectomized women and 10 agematched normotensive women. The mean basal diastolic BP was slightly higher in the adrenalectomized women (80 vs. 68 mm Hg; P < 0.05). During mental arithmetic, the adrenalectomized women had a smaller heart rate increase than the normal women [6 ± 1% (±SE) vs. 16 ± 4%; P < 0.05], but the BP response was not different. During the head-up tilt and cold pressor tests the hemodynamic responses were similar in the adrenalectomized and normal women. As expected, plasma E was undetectable in the adrenalectomized women. Plasma norepinephrine (NE) did not change in either group during mental arithmetic. In the adrenalectomized women the plasma NE increases during the head-up tilt and cold pressor test were not significantly different from those in the normal women. Thus, the adrenalectomized women had a normal pressor response during all 3 types of adrenergic stimulation, apparently independent of plasma E. Together with the normal plasma NE responses to head-up tilt and cold exposure, we challenge the contention that the E-mediated presynaptic β-adrenergic stimulation of NE release plays a pivotal physiological role during short term adrenergic stress.

* This work was supported in part by a grant from The Netherlands Heart Foundation (Grant 82064) and the University Research Pool, Nijmegen.

Received November 2, 1987.




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Copyright © 1988 by The Endocrine Society