RESUMO
Acetylcholine acts via presynaptic receptors to inhibit adrenergic neurotransmission in vascular tissue. To test the possibility that this modulation might be altered by hyperactivity of the sympathetic nervous system, rats were exposed to cold stress for 5 days. Rat caudal (tail) arteries were excised, cannulated and perfused at constant flow. Responses to transmural nerve stimulation and/or acetylcholine were measured. In arteries from nonstressed rats, acetylcholine produced a dose-dependent inhibition of responses to nerve stimulation of 10 Hz. Likewise, acetylcholine (32 ng/ml) produced a frequency-dependent inhibition to nerve stimulation. Cold stress elevated sympathetic nerve activity in the tail artery as indicated by increased tyrosine hydroxylase activity. Responses to exogenous norepinephrine alone were not different between arteries from cold-stressed and nonstressed rats. In arteries from cold-stressed rats, acetylcholine inhibited the response to nerve stimulation in a dose-dependent manner and at each dose of acetylcholine the inhibition was greater than in arteries from nonstressed rats. Likewise, the inhibition of the frequency-dependent responses to nerve stimulation by acetylcholine was greater in arteries from cold-stressed than from nonstressed rats. These data show that after chronic elevation of vasomotor tone, acetylcholine is a more effective modulator of neurogenic tone which indicates the development of the functional equivalent of supersensitivity of presynaptic receptor-mediated events.
