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J Appl Physiol (October 17, 2003). doi:10.1152/japplphysiol.00852.2003
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Submitted on August 12, 2003
Accepted on October 13, 2003

Functional Magnetic Resonance Signal Changes in Neural Structures to Baroreceptor Reflex Activation

Luke A Henderson1, Chris A Richard2, Paul M Macey2, Matthew L Runquist3, Pearl L Yu2, Jean-Philippe Galons3, and Ronald M Harper4*

1 Anatomy and Histology, University of Sydney, Sydney, NSW, Australia; Neurobiology, University of California at Los Angeles, Los Angeles, CA, USA
2 Neurobiology, University of California at Los Angeles, Los Angeles, CA, USA
3 Radiology, University of Arizona, Tucson, AZ, USA
4 Neurobiology, University of California at Los Angeles, Los Angeles, CA, USA; Brain Research Institute, University of California at Los Angeles, Los Angeles, CA, USA

* To whom correspondence should be addressed. E-mail: rharper{at}ucla.edu.

The sequence of neural responses to exogenous arterial pressure manipulation remains unclear, especially for extramedullary sites. We used functional magnetic resonance imaging procedures to visualize neural responses during pressor (phenylephrine) and depressor (sodium nitroprusside) challenges in seven, isoflurane-anesthetized, adult cats. Depressor challenges produced signal intensity declines in multiple cardiovascular-related sites in the medulla, including the nucleus tractus solitarius, caudal and rostral ventrolateral medulla. Signal decreases also emerged in the cerebellar vermis, inferior olive, dorsolateral pons, and right insula. Rostral sites, such as the amygdala and hypothalamus, increased signal intensity as arterial pressure declined. In contrast, arterial pressure elevation elicited smaller signal increases in medullary regions, the dorsolateral pons, and the right insula, and signal declines in regions of the hypothalamus, with no change in deep cerebellar areas. Responses to both pressor and depressor challenges were typically lateralized. In a subset of animals, barodenervation resulted in comparable rises and falls of blood pressure to the pharmacologic challenges, but different regional neural responses, indicating that the regional signal intensity responses did not derive from global perfusion effects but from baroreceptor mediation of central mechanisms. The findings demonstrate widespread, lateralized distribution of neural sites responsive to blood pressure manipulation. The distribution and time course of neural responses follow patterns associated with early and late compensatory reactions.




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