alexa Change in central kinin B2 receptor density after exercise training in rats.


Neurochemistry & Neuropharmacology

Author(s): Caetano AL, Viel TA, Bittencourt MF, Araujo MS, De Angelis K, , Caetano AL, Viel TA, Bittencourt MF, Araujo MS, De Angelis K, , Caetano AL, Viel TA, Bittencourt MF, Araujo MS, De Angelis K, , Caetano AL, Viel TA, Bittencourt MF, Araujo MS, De Angelis K,

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Abstract Cardiovascular responses elicited by the stimulation of kinin B2 receptors in the IV cerebral ventricle, paratrigeminal nucleus or in the thoracic spinal cord are similar to those observed during an exercise bout. Considering that the kalikrein-kinin system (KKS) could act on the cardiovascular modulation during behavioral responses as physical exercise or stress, this study evaluated the central B2 receptor densities of Wistar (W) and spontaneously hypertensive rats (SHR) after chronic moderate exercise. Animals were exercise-trained for ten weeks on a treadmill. Afterwards, systolic blood pressure decreased in both trained strains. Animals were killed and the medulla and spinal cord extracted for B2 receptor autoradiography. Trained animals were compared to their sedentary controls. Sedentary groups showed specific binding sites for Hoe-140 (fmol/mg of tissue) in laminas 1 and 2 of the spinal cord, nucleus of the solitary tract (NTS), area postrema (AP), spinal trigeminal tract (sp5) and paratrigeminal nucleus (Pa5). In trained W a significant increase (p<0.05) in specific binding was observed in the Pa5 (31.3\%) and NTS (28.2\%). Trained SHR showed a significant decrease in receptor density in lamina 2 (21.9\%) of the thoracic spinal cord and an increase in specific binding in Pa5 (36.1\%). We suggest that in the medulla, chronic exercise could hyper stimulate the KKS enhancing their efficiency through the increase of B2 receptor density, involving this receptor in central cardiovascular control during exercise or stress. In the lamina 2, B2 receptor might be involved in the exercise-induced hypotension. Copyright © 2010 Elsevier B.V. All rights reserved. This article was published in Auton Neurosci and referenced in Neurochemistry & Neuropharmacology

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