| Catecholamine (CA) systems within the central nervous system play an important role in cardiovascular regulation in adult mammals, and may be critical for normal cardiovascular development. Depletions of central CAs in infancy or adulthood reportedly alter a number of cardiovascular parameters, although the manifestation of these alterations may differ depending on the timing of the depletions, and of testing. The present experiments addressed the following questions: (1) Do central CA depletions sustained in infancy disrupt tonic or reflexive cardiovascular function in awake, freely moving rats? (2) Do the cardiovascular consequences of these depletions change during development? (3) Do central CA depletions have similar cardiovascular consequences when sustained in adulthood?;Infant (first postnatal week) or adult (90-120 days of age) rats were given intracisternal injections of 6-hydroxydopamine (6-HDA) or its vehicle solution. The 6-HDA treatment produced large, permanent depletions of brainstem and forebrain CAs. Cardiac norepinephrine was reduced in animals treated with 6-HDA as infants. Chronic measurements of arterial blood pressure, heart rate, and heart rate variability associated with respiration (respiratory sinus arrhythmia, RSA) were obtained via indwelling carotid catheters. Animals depleted as adults evidence normal heart rate, blood pressure and RSA under baseline conditions and following autonomic blockade with atenolol or scopolamine methyl nitrate. Reflex bradycardia in response to hypertension (the baroreflex) induced by phenylephrine was not significantly altered. Similarly, there was no evidence of cardiovascular dysfunction in weanling animals (30-33 days of age) that were depleted as infants. In contrast, when animals depleted as infants were tested as adults, baseline blood pressure was significantly reduced. Moreover, the pattern of cardiac response to an auditory stimulus was disrupted by the depletion.;These results demonstrate: (1) that early depletions of central CAs alter the development of cardiovascular regulation, (2) that the expression of these deficits changes during development, and (3) that the effects may differ depending the timing of the CA depletions. |
