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Brain insulin modulates the cardiovascular response to central command and exercise pressor reflex stimulation in rats
Author(s) -
Mizuno Masaki,
Downey Ryan,
Mitchell Jere H,
Smith Scott A
Publication year - 2012
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.26.1_supplement.1091.12
Subject(s) - medicine , insulin , endocrinology , stimulation , skeletal muscle , reflex , blood pressure , contraction (grammar) , central nervous system , heart rate
Evidence demonstrates that insulin not only regulates glucose metabolism but also neural activity within the brain. Neural input from central command (CC) and the skeletal muscle exercise pressor reflex (EPR) to cardiovascular regulatory centers within the brain contribute importantly to the control of the circulation during exercise. However, whether brain insulin modulates CC and EPR activity remains undetermined. Brain insulin inhibits hypothalamic neural activity and decreases the blood pressure response to brain stem stimulation. Thus, we hypothesized that brain insulin attenuates the circulatory response to activation of CC and the EPR. To test this hypothesis, the cardiovascular responses to stimulation of the mesencephalic locomotor region (CC activation) and contraction of hindlimb skeletal muscle (EPR activation) were measured in decerebrate Sprague‐Dawley rats before and 60 min after intracerebroventricular injection of insulin (0.25 U/kg). Insulin administration reduced the mean arterial pressure and heart rate responses to stimulation of the mesencephalic locomotor region (change from baseline: 71 ± 20 vs. 25 ± 19 mmHg; 8 ± 3 vs. 3 ± 1 bpm, respectively) as well as skeletal muscle contraction (change from baseline: 56 ± 13 vs. 25 ± 9 mmHg; 17 ± 5 vs. 6 ± 4 bpm, respectively). The results suggest that both CC and EPR activity can be attenuated by insulin within the brain. Supported by NIH HL‐088422