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Clonidine‐evoked respiratory effects in anaesthetized rats
Author(s) -
Kaczyñska Katarzyna,
SzeredaPrzestaszewska Małgorzata
Publication year - 2006
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.2005.031914
Subject(s) - clonidine , anesthesia , vagotomy , respiratory system , respiratory rate , medicine , tidal volume , carotid sinus , stimulation , blood pressure , heart rate , reflex
The respiratory effects of stimulation of α 2 ‐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 μg 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 α 2 ‐adrenergic receptors with intravenous doses of SKF 86466 (200 μg 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 α 2 ‐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.