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Cardiovascular responses induced by excitation/lesion of caudal paramedial medulla (CPM)
Author(s) -
Mortati Maria Carolina Galli,
Seiji Willian Korim,
Rosa Daniel Alves,
Cravo Sergio L
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.737.25
Subject(s) - microinjection , vasoconstriction , medicine , heart rate , medulla , mean arterial pressure , rostral ventrolateral medulla , blood pressure , medulla oblongata , lesion , cardiology , endocrinology , anesthesia , chemistry , anatomy , central nervous system , surgery
Previous studies suggested that neurons located in the midline and adjacent regions of the caudal medulla participate in cardiovascular regulation. Presently we sought to determine the effects of chemical excitation or lesion of this area. Male Wistar rats were anesthetized, paralized, and artificially ventilated and prepared for mean arterial pressure (MAP), heart rate (HR), and blood flow (BF) recordings. Hindquarter (HQVC) and renal vascular conductance (RVC) were determined by the ratio MAP/BF. Bilateral microinjection of KA (5 Mm, 50 nL) into CPM (1.6 rostral, 0.5 lat and −2.3 mm to the CS) increased MAP (+43±10.3 mmHg), HR (+48±23.6 bpm) and induced renal and hindquarter vasoconstriction (−72±8.3; −75±3.6% of baseline, respectively). Reversely, bilateral microinjection of ibotenic acid (2.5nM, 50nL) induced hypotension (−41±13.3 mmHg) and bradicardia (−75±43.1 bmp) without significant changing RVC or HVC (2±12.8; 33±29.2% of baseline respectively). Forty minutes after IBO microinjection of KA into the same sites overturned these effects, inducing marked hypertension (+38±13.7 mmHg), tachycardia (43±8.3 bpm) and renal and hindlimb vasoconstriction (−74±5.9,−75±6.4% of baseline, respectively). These results suggested that paramedial medulla contains excitatory and inhibitory cardiovascular pathways that may be differentiated by their sensitivity to glutamate agonists.