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Cold Pressor Test: Medullo‐Spinal Pathways and Neurotransmitters
Author(s) -
Nakamura Takeshi,
Sapru Hreday N
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1169.6
Subject(s) - ionotropic effect , rostral ventrolateral medulla , cold pressor test , anesthesia , spinal cord , vagotomy , heart rate , glutamate receptor , medicine , blood pressure , endocrinology , chemistry , receptor , psychiatry
The neural pathways and transmitters that mediate pressor and tachycardic responses to the cold pressor test are not firmly established. The present experiments were designed to delineate these pathways. Experiments were carried out on urethane‐anesthetized, artificially ventilated, barodenervated, male, Wistar rats. The rats were fixed in a stereotaxic instrument and placed in a plexiglass rectangular dish. Ice‐cold water was rapidly poured into the dish to immerse the ventral half of the rat's body and then removed by rapid suction. Cold water immersion for 2 min elicited an increase in mean arterial pressure (40–46 mmHg) and heart rate (60–76 bpm). Bilateral vagotomy had no significant effect on the pressor responses but significantly reduced the tachycardic responses. Bilateral blockade of ionotropic glutamate receptors (IGLURs), by injections of D‐AP7 and NBQX, in the rostral ventrolateral medullary pressor area (RVLM) or the spinal cord significantly decreased the pressor responses. HR responses remaining after the blockade of IGLURs in the spinal cord were abolished after bilateral vagotomy. These results indicate that: 1) the pressor and tachycardic responses to cold pressor test are mediated by ionotropic glutamate receptors in the RVLM and the spinal cord, and 2) inhibition of the vagal input to the heart also contributes to the tachycardic responses. Support: NIH grants HL 024347 and HL076248.