Cardioinhibitory actions of clonidine assessed by cardiac vagal motoneuron recordings.

Emil Toader (1) , Andrei Cividjian (1) , Nicolas Rentero (1) , Robin M Mcallen (2) , Luc Quintin (1)

1 PICM - Physiologie intégrative, cellulaire et moléculaire
2 Howard Florey Institute

BACKGROUND: Cardiac vagal activity is now considered as an important therapeutic target. However, there is a lack of direct data on how cardiac vagal motoneurons respond to parasympathomimetic agents. METHODS: Rats were anesthetized with urethane and mechanically ventilated. Single-unit activity was recorded in the nucleus ambiguus from cardiac vagal motoneurons, identified by antidromic activation from the cardiac vagal branch and their barosensitivity. RESULTS: Nitroprusside lowered systolic blood pressure, increased heart rate and inhibited cardiac vagal motoneuron activity (n = 5 cells in five rats). Clonidine 1-100 microg kg(-1) intravenously, however, lowered systolic blood pressure, but it increased cardiac vagal motoneuron activity (n = 8 cells in eight rats). It also enhanced their barosensitivity. An unsuspected further finding was that clonidine significantly increased the occurrence of cardiac vagal motoneuron firing spikes separated by short (< 30 ms) interspike intervals ('doublet'). CONCLUSION: Such grouped patterns are known to enhance neurotransmitter release. Therefore, these data provide a new mechanism by which clonidine can further potentiate parasympathetic actions on the heart.

Mots clés: baroreceptor-heart rate reflex; clonidine; firing pattern; gain; nitroprusside; single-unit activity; [alpha]-2 agonist; baroreflex; cardiac vagal motoneuron; cardiac vagal preganglionic neuron

Domaines: Autre [q-bio.OT]

Emil Toader, Andrei Cividjian, Nicolas Rentero, Robin M Mcallen, Luc Quintin. Cardioinhibitory actions of clonidine assessed by cardiac vagal motoneuron recordings.. Journal of Hypertension, 2008, 26 (6), pp.1169-80. ⟨10.1097/HJH.0b013e3282fd10e0⟩. ⟨hal-00302351⟩