학술논문

Cardiovascular and neurohormonal responses to i. v. l-arginine in two groups with primary autonomic failure
Document Type
Author abstract
Source
Journal of Neurology. Dec, 2001, Vol. 248 Issue 12, p1036, 6 p.
Subject
United Kingdom
Language
English
ISSN
0340-5354
Abstract
Byline: J. Kimber (2), L. Watson (2), C. J. Mathias (1) Keywords: Key words Autonomic failure; L-arginine; Neurohormonal Abstract: Nitric oxide (NO) is synthesised from the amino-acid l-arginine by the enzyme nitric oxide synthetase (NOS) and modulates a wide variety of neural, cardiovascular and hormonal processes. Cardiovascular autonomic dysfunction and impaired neurohormonal secretion characterise patients with primary chronic autonomic failure (AF). To investigate the role of NO, we studied the cardiovascular and neurohormonal effects of intravenous (i. v.) l-arginine (0.5 g/kg) in 20 patients with AF: [10 with multiple system atrophy (MSA) and 10 patients with pure autonomic failure (PAF)] and compared them with age-matched healthy normal subjects. Basal mean arterial pressure (MAP) was higher in MSA and PAF than controls (p < 0.02). Following l-arginine, MAP fell in MSA (mean: -39 +- 8 mmHg, 95 % CI -21 to -57, p < 0.05) and PAF (-37 +- 5, 95 % CI -26 to -58, p < 0.05) but not in controls. There were no significant changes in HR between the groups. Basal plasma noradrenaline (NA) was similar in controls and MSA, but lower in PAF (p < 0.05). Following l-arginine the percentage rise in plasma NA was similar in controls and MSA, but not in PAF (p < 0.05). Plasma insulin rose similarly in controls and MSA, but was higher in PAF (p < 0.05). Plasma glucose rose to a similar level in all groups. In conclusion, l-arginine, lowered BP in both MSA and PAF. In PAF a contributory factor may be increased insulin release, without a compensatory increase in sympatho-neural activity to counter its potential vasodilator effects. These studies suggest that reducing NO levels, as with NOS inhibitors, may be of benefit in the treatment of postural hypotension and possibly post-prandial hypotension in chronic primary AF. Author Affiliation: (1) Neurovascular Medicine Unit, Imperial College of Science, Technology and Medicine, St Mary's Hospital, Praed St, London W2 1NY, UK, Tel.: ++41-02 07-8 86 14 68, Fax: ++41-02 07-8 86 15 40, E-Mail: cjmathias@ic.ac.uk, GB (2) Autonomic Unit, National Hospital for Neurology and Neurosurgery, Queen Square and University Department of Neurology, Institute of Neurology, University College London, London, GB Article note: Received: 3 May 2000, Received in revised form: 13 September 2000, Accepted: 22 January 2001