Received August 11, 2005
Revised September 16, 2005
Accepted after revision November 7, 2005

¹ PAS Medical Research Centre

^* To whom correspondence should be addressed. E-mail: kkacz{at}cmdik.pan.pl.

	Abstract

Respiratory effects of 2-adrenergic receptors' stimulation were studied in spontaneously breathing anaesthetized rats that were either neurally intact, or bilaterally vagotomised, or subject to bilateral combined midcervical vagotomy and carotid sinus nerves' section. Intravenous clonidine bolus (15 mg/kg) 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 the carotid sinus nerves' section, clonidine challenge continued to decrease the respiratory rate, but not the tidal volume. Blockade of 2--adrenergic receptors with intravenous SKF 86466 doses (200 µg/kg) 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 pre-challenge value. The SKF 86466 pre-treatment lowered mean arterial blood pressure control values and reduced the magnitude of post-clonidine changes. These results indicate that: (i) clonidine-evoked activation of 2-adrenergic receptors affects differently both components of the breathing pattern, which effect occurs beyond the lung vagi; (ii) changes in tidal volume result from carotid bodies' excitation and are coupled with centrally mediated slowing of the respiratory rhythm. Key words: carotid body, 2-adrenergic receptors, control of breathing, rat, clonidine

Key Words: Adrenoceptor, Rat, Respiration