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© 1990 Oxford University Press

research-article

Is Orthostatic Hypotension in the Elderly due to Autonomic Failure?

B. J. ROBINSON, L. I. STOWELL, R. H. JOHNSON* and K. T. PALMER

Neurological Research Group, Wellington School of Medicine, Wellington Hospital Wellington, New Zealand
Office of the Director of Postgraduate Medical Education and Training, John Radcliffe Hospital Headington, Oxford 0X3 9DU

* Address correspondence to Dr R. H. Johnson

In order to investigate whether orthostatic hypotension in elderly people is due to autonomic nervous system dysfunction or blood vessel abnormalities, we have measured platelet and lymphocyte adrenoceptor numbers and agonist binding in addition to venous plasma catecholamine concentrations. Eight elderly subjects with orthostatic hypotension and six control elderly subjects were studied. None of the subjects had other symptoms of autonomic failure. There was no significant difference between the heart rate or plasma catecholamine responses to standing of the two groups. The orthostatic hypotension subjects had a significant rise of their plasma vasopressin levels whereas the control group had no significant change. The number of {alpha}2-adrenoceptor sites in platelets was lower in the orthostatic hypotensive group compared to the controls and the binding affinity was greater than in the controls. There were no significant differences in ß-adrenoceptor binding sites or affinities in isolated lymphocytes between the two groups.

The similar changes in heart rate and catecholamines together with the vasopressin changes suggest that, in these elderly patients with an abnormal drop of blood pressure on standing, there is no dysfunction of autonomic pathways concerned with cardiovascular function. The lower numbers of {alpha}2-adrenoceptor sites on isolated platelets in subjects with orthostatic hypotension could indicate reduced {alpha}2-adrenoceptor numbers on their blood vessels which could contribute to their inability to maintain blood pressure while standing.

Received November 21, 1989;
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