Abstract
We compared the mean arterial pressure and heart rate activity of conscious, unrestrained rats during 1-hour and 24-hour continuous recording sessions, 3 to 4 weeks after either sinoartic denervation, placement of electrolytic lesions in the nucleus tractus solitarii, or sham operations. Sinoaortic denervation and nucleus tractus solitarii lesions both eliminated the reflex bradycardia to a phenylephrine-induced pressor response. No difference was found in the average level and lability of the mean arterial pressure between 1-hour and 24-hour recordings for any group. No elevation in the average mean arterial pressure of rats with nucleus tractus solitarii lesions was observed, although a mild hypertension was noted in half the sinoarotic-denervated rats, while the other half were normotensive. Group differences were not found for heart rate or heart rate variability; however, 24-hour recordings yielded significantly higher values than 1-hour recordings for all groups. Both medullary lesions and sinoaortic denervation significantly increased the lability of the mean arterial pressure, but the magnitude of the increase was significantly greater in the rats with lesions. The lability of the mean arterial pressure in sinoaortic-denervated rats depended largely on movement-related depressor responses that produced a negative skew in the frequency distribution of their mean arterial pressure. Rats with nucleus tractus solitarii lesions exhibited both pressor and depressor responses that resulted in pressure distributions that had a slight positive skew similar to that displayed by control rats. It is concluded that short-term continuous recordings of mean arterial pressure and heart rate accurately estimate the altered cardiovascular activity of baroreceptor-denervated rats. The differences in the cardiovascular responses of central and peripheral baroreceptor-denervated rats are believed to be due to the more extensive destruction by nucleus tractus solitarii lesions of central neurons and pathways involved in cardiovascular regulation.
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