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.
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.
Authors: Paolo Castiglioni; Gianfranco Parati; Marco Di Rienzo; Roberta Carabalona; Andrei Cividjian; Luc Quintin Journal: J Physiol Date: 2010-11-29 Impact factor: 5.182
Authors: Alberto Porta; Paolo Castiglioni; Marco Di Rienzo; Vlasta Bari; Tito Bassani; Andrea Marchi; Maddalena Alesssandra Wu; Andrei Cividjian; Luc Quintin Journal: Auton Neurosci Date: 2013-03-27 Impact factor: 3.145
Authors: D Longrois; F Petitjeans; O Simonet; M de Kock; M Belliveau; C Pichot; Th Lieutaud; M Ghignone; L Quintin Journal: Rom J Anaesth Intensive Care Date: 2021-01-04