Clonidine‐evoked respiratory effects in anaesthetized rats

Abstract

The respiratory effects of stimulation of alpha2-adrenergic receptors were studied in spontaneously breathing anaesthetized rats that were neurally intact, or bilaterally vagotomized, or subjected to bilateral combined midcervical vagotomy and section of the carotid sinus nerves. An intravenous clonidine bolus (15 microg kg(-1)) evoked a prolonged slowing of the respiratory rate in all the neural states explored. Vagotomy reduced the early clonidine-evoked decline, but not the augmentation of tidal volume that followed the decline. After section of the carotid sinus nerves, clonidine challenge continued to decrease the respiratory rate, but not the tidal volume. Blockade of alpha2-adrenergic receptors with intravenous doses of SKF 86466 (200 microg kg(-1)) abolished all respiratory effects of the clonidine challenge. In all the neural states studied, clonidine evoked a significant short-lived rise in mean arterial blood pressure followed by a decrease below the respective prechallenge value. The SKF 86466 pretreatment lowered mean arterial blood pressure control values and reduced the magnitude of postclonidine changes. These results indicate that: (i) clonidine-evoked activation of alpha2-adrenergic receptors affects the two components of the breathing pattern differently, and this occurs beyond the lung vagi; and (ii) changes in tidal volume result from excitation of the carotid bodies and are coupled with centrally mediated slowing of the respiratory rhythm.