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J Appl Physiol (1985). 2007 Aug;103(2):646-54. Epub 2007 Jun 7.

Linear acceleration-evoked cardiovascular responses in awake rats.

Author information

1
Dept. of Otolaryngology and Communicative Sciences, University of Mississippi Medical Center, Jackson, MS 39216, USA. hozhu@ent.umsmed.edu

Abstract

It has been well documented that vestibular-mediated cardiovascular regulation plays an important role in maintaining stable blood pressure (BP) during postural changes. But the underlying neural mechanisms remain to be elucidated. In particular, because the vestibular stimulation employed in previous animal studies activated both semicircular canals and otolith organs, the contributions of the otolith system has not been studied selectively. The goal of the present study was to characterize cardiovascular responses to natural otolith stimulation in awake rats that were subjected to pure linear motion. In any of the four directions tested, transient linear motion produced a short-latency ( approximately 520 ms) increase in mean BP with a peak of 8.27 +/- 0.66 mmHg and was followed by a decrease in BP. There was an initial small biphasic response in heart rate (HR) that was followed by a longer duration increase. The short-latency increase in BP was absent in rats that were pentobarbital sodium anesthetized or that were labyrinthectomized bilaterally, but it was unaffected by baroreceptor denervation, indicating that it was of otolith origin. The increase in BP was linear acceleration intensity dependent and was not affected by absence of visual cues. Furthermore, the BP response was attenuated by inactivation of the medial and inferior vestibular nuclei by microinjections of muscimol, indicating that the otolith-driven cardiovascular responses are mediated by the neurons in these areas. These results not only demonstrate the otolith specific influences on the cardiovascular system but also they establish the first rodent model for examining the neural mechanisms underlying the otolith-mediated cardiovascular regulation.

PMID:
17556494
DOI:
10.1152/japplphysiol.00328.2007
[Indexed for MEDLINE]
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