Abstract
Isometric muscle contractions cause an increase in mean arterial pressure and heart rate. Previously, we showed that substance P (SP) is released from sites in the feline medial nucleus tractus solitarius (mNTS) in response to isometric muscle contractions, and that it most likely interacted with NK1 tachykinin receptors at these sites. This study was undertaken to determine whether other tachykinin receptors in this area of the brainstem are involved with the muscle pressor response. Receptor autoradiography, using [125I]Bolton-Hunter SP and [125I] [MePhe7] neurokinin B to label NK1 and NK3 receptors, respectively, indicated that NK3 tachykinin receptors are as abundant as NK1 and NK3 receptors, respectively, indicated that NK3 tachykinin receptors are as abundant as NK1 receptors in this region of the feline brainstem Injections of the specific NK3 receptor antagonist, SR 142801 (0.1 to 10μM) into the mNTS did not modify the pressor response or the heart rate response to isometric muscle contractions. Injection of SR142801 into the NTS prior to the injection of the NK1 antagonist, GR82334 did not affect the action of GR82334 to attenuate the muscle pressor reflex. We conclude that NK3 receptors in the NTS are not involved with the regulation of cardiovascular function during activation of the muscle pressor response.
Published Version
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