title: Functional magnetic resonance signal changes in neural structures to baroreceptor reflex activation.
abstract: 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, and 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 rises and falls of blood pressure that were comparable to these resulting from the pharmacological 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.
authors.affiliation: Department of Neurobiology, University of California at Los Angeles, Los Angeles, California 90095-1763, USA.
authors.forename: Luke A
authors.initials: LA
authors.lastname: Henderson
authors.forename: Chris A
authors.initials: CA
authors.lastname: Richard
authors.forename: Paul M
authors.initials: PM
authors.lastname: Macey
authors.forename: Matthew L
authors.initials: ML
authors.lastname: Runquist
authors.forename: Pearl L
authors.initials: PL
authors.lastname: Yu
authors.forename: Jean-Philippe
authors.initials: JP
authors.lastname: Galons
authors.forename: Ronald M
authors.initials: RM
authors.lastname: Harper
mesh_terms: D000758:Anesthesia; D000818:Animals; D001013:Aorta, Thoracic / Q000502:physiology; D017704:Baroreflex / Q000187:drug effects / Q000502:physiology*; D001794:Blood Pressure / Q000502:physiology*; D002346:Carotid Sinus / Q000502:physiology; D002415:Cats; D002531:Cerebellum / Q000502:physiology; D002540:Cerebral Cortex / Q000502:physiology; D005260:Female; D007839:Functional Laterality / Q000502:physiology; D006339:Heart Rate / Q000502:physiology; D007031:Hypothalamus / Q000502:physiology; D008279:Magnetic Resonance Imaging; D008297:Male; D010656:Phenylephrine / Q000494:pharmacology; D011149:Pons / Q000502:physiology; D012965:Sodium Chloride; D017552:Solitary Nucleus / Q000502:physiology*; D013562:Sympathectomy; D013564:Sympathetic Nervous System / Q000502:physiology; D013566:Sympathomimetics / Q000494:pharmacology
chemical_list: D013566:Sympathomimetics; D010656:Phenylephrine; D012965:Sodium Chloride