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NEUROLOGY 1992;42:590
© 1992 American Academy of Neurology

Hypotension-induced vasopressin release distinguishes between pure autonomic failure and multiple system atrophy with autonomic failure

H. Kaufmann, MD, E. Oribe, MD, M. Miller, MD, P. Knott, PhD, M. Wiltshire-Clement, BA and M. D. Yahr, MD

Autonomic Nervous System Laboratory, Departments of Neurology, Mount Sinai School of Medicine, New York, NY (Drs. Kaufmann, Oribe and Yahr)
Geriatrics and Adult Development, Mount Sinai School of Medicine, New York, NY (Dr. Miller and M. Wiltshire-Clement)
Neurochemistry Laboratory, Mount Sinai School of Medicine, New York, NY (Dr. Knott).

To investigate whether activation of afferent and central baroreceptor pathways could differentiate between pure autonomic failure (PAF) and multiple system atrophy with autonomic failure (MSA), we determined the effect of upright tilt on circulating levels of vasopressin in patients with PAF and patients with MSA. We also studied 14 normal subjects, nine of whom developed acute hypotension due to vasovagal syncope. In patients with PAF and in normal subjects with vasovagal syncope, upright tilt induced marked hypotension and a pronounced increase in the plasma concentration of vasopressin (1.1 ± 0.3 to 38.0 ± 8.0 pmol/l in PAF and 1.0 ± 0.2 to 27.4 ± 7.2 pmol/l in vasovagal syncope, p < 0.005 for both). In patients with MSA, upright tilt also elicited profound hypotension but circulating levels of vasopressin increased little (0.5 ± 0.1 to 1.5 ± 0.3 pmol/l, p < 0.05). During upright tilt, the plasma concentration of norepinephrine significantly increased in normal subjects but did not increase in patients with autonomic failure. Our results indicate that afferent and central baroreceptor pathways involved in vasopressin release are normal in patients with PAF but are impaired in patients with MSA. Thus, measurement of baroreceptor-mediated vasopressin release appears to provide a clear marker to differentiate between patients with PAF and patients with MSA.

Address correspondence and reprint requests to Dr. Horacio Kaufmann, Department of Neurology, Mount Sinai School of Medicine, New York, NY 10029.

Supported in part by NIH grants #NS007245 and M01-RR00071.

Presented in part at the 41st annual meeting of the American Academy of Neurology, Boston, MA, April 1991.

Received June 28, 1991. Accepted for publication in final form August 27, 1991.




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