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Neonatal NGF antiserum abolishes sympathetic vascular responses in rats; leaves open whether growth factor modulation could target human autonomic cardiovascular control.
Sympathetic function and cardiovascular responses were measured in rats treated at birth with an antiserum developed to the sympathetic nerve growth factor. The intact animals exhibited ptosis, miosis, and decreased excretion of norepinephrine in the urine. Electrical stimulation of the sympathetic innervation to the vessels of the perfused hindquarters failed to produce vasoconstriction or vasodilatation in any of the treated rats over a wide range of stimulus parameters. Alterations in vascular reactivity characteristic of sympathetic denervation were noted; responsiveness was increased to norepinephrine but not to other constrictor agents. Chemical stimulation of the sympathetic ganglia with 1,1-dimethyl-4-phenyl-piperazinium iodide (DMPP) did not activate the postganglionic fibers but did promote the release of catecholamines from the adrenal medulla. The treated rats showed elevated resistance to flow in the hindquarters. The results of this investigation thus demonstrate that treatment with the antinerve growth factor effectively abolishes vasomotor function of the fibers of the sympathetic nervous system.
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Brody et al. (1964) studied this question.
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