Recruitment of cardiac parasympathetic activity: effects of clonidine on cardiac vagal motoneurones, pressure lability, and cardiac baroreflex slope in rats

Toader, Emil; Cividjian, Andrei; Quintin, Luc

doi:10.1093/bja/aen390

Cited by 14 publications

(10 citation statements)

References 48 publications

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“…Ketanserin reduced the incidence of fatal strokes, through amelioration of BRS besides reduction of BP [76,151]. Other drugs, such as clonidine, moxonidine, mecobalamin, and folic acid, also improved BRS [152–155]. Baroreceptor stimulation has been used in patients with drug‐resistant hypertension [156].…”

Section: Strategies Of Stroke Prevention In Patients With Hypertensionmentioning

confidence: 99%

From Hypertension to Stroke: Mechanisms and Potential Prevention Strategies

Zhou

Cai

2011

CNS Neuroscience & Therapeutics

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SUMMARYStroke is a major cause of disability and death worldwide. Prevention aimed at risk factors of stroke is the most effective strategy to curb the stroke pandemic. Hypertension is one of the most important risk factors for stroke. Despite the substantial evidence of the benefits of lowering blood pressure, conventional treatment does not normalize the burden of major cardiovascular events in patients with hypertension. Fully understanding the factors involved in the hypertension-induced stroke helps to develop new strategies for stroke prevention. Antihypertensive therapies selected should have positive blood pressureindependent effects on stroke risk. This review summarizes the factors involved in the hypertension-induced stroke, such as oxidative stress, inflammation, and arterial baroreflex dysfunction, and potential strategies for its prevention, therefore, provides clues for clinicians.

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Section: Strategies Of Stroke Prevention In Patients With Hypertensionmentioning

confidence: 99%

From Hypertension to Stroke: Mechanisms and Potential Prevention Strategies

Zhou

Cai

2011

CNS Neuroscience & Therapeutics

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“…65,66 Most recently, clonidine was shown to increase the activity of baroreceptive neurons in the ventrolateral medulla, enhance the slope of the cardiac baroreflex, and reduce pressure lability. 67 New devices stimulating baroreceptors are emerging in the treatment of chronic refractory hypertension. Mediated through the central sympathoinhibitory effect by stimulating the carotid baroreceptors electrically, these devices ameliorate baroreflex sensitivity and reduce hypertension.…”

Section: Baroreflex Modulation: a New Therapeutic Target In Stroke?mentioning

confidence: 99%

Baroreflex: A New Therapeutic Target in Human Stroke?

Sýkora

Diedler

Turčãni

et al. 2009

Stroke

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Background and Purpose-Autonomic dysfunction, including increased sympathetic drive and blunted baroreflex, has repeatedly been observed in acute stroke. Of clinical importance is that the stroke-related autonomic imbalance seems to be linked to worse outcome after stroke. Here, we discuss the role of baroreflex impairment in acute stroke and its possible pathophysiological and therapeutic relevance. Summary of Review-Possible mechanisms linking baroreflex impairment with unfavorable outcome in stroke may include increased cardiovascular morbidity and mortality, promotion of secondary brain injury due to local inflammation, hyperglycemia, or altered cerebral perfusion. Conclusions-We suggest therefore that the modifying of autonomic functions may have important therapeutic implications in acute ischemic as well as in hemorrhagic stroke. (Stroke. 2009;40:e678-e682.)

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“…Activation of α 2 adrenergic receptors in the central nervous system evokes a diverse range of physiological effects, including reducing blood pressure and increasing sinus arrhythmia(Toader et al, 2009). Activation of α 2 adrenergic receptors with agonists, such as clonidine, inhibits adenylyl cyclase activity, resulting in a decrease in presynaptic Ca 2+ concentrations and inhibition of norepinephrine release.…”

Section: Introductionmentioning

confidence: 99%

Clonidine, an α2-receptor agonist, diminishes GABAergic neurotransmission to cardiac vagal neurons in the nucleus ambiguus

2010

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In hypertension there is an autonomic imbalance in which sympathetic activity dominates over parasympathetic control. Parasympathetic activity to the heart originates from cardiac vagal neurons located in the nucleus ambiguus. Pre-sympathetic neurons that project to sympathetic neurons in the spinal cord are located in the ventral brainstem in close proximity to cardiac vagal neurons, and many of these pre-sympathetic neurons are catecholaminergic. In addition to their projection to the spinal cord, many of these pre-sympathetic neurons have axon collaterals that arborize into neighboring cardio-respiratory locations and likely release norepinephrine onto nearby neurons. Activation of α 2 adrenergic receptors in the central nervous system evokes a diverse range of physiological effects, including reducing blood pressure. This study tests whether clonidine, an α 2 adrenergic receptor agonist, alters excitatory glutamatergic, and/or inhibitory GABAergic or glycinergic synaptic neurotransmission to cardiac vagal neurons in the nucleus ambiguus. Cardiac vagal neurons were identified in a in-vitro brainstem slice preparation and synaptic events were recording using whole cell voltage clamp methodologies. Clonidine significantly inhibited GABAergic neurotransmission, but had no effect on glycinergic or glutamatergic pathways to cardiac vagal neurons. This diminished inhibitory GABAergic neurotransmission to cardiac vagal neurons would increase parasympathetic activity to the heart, decreasing heart rate and blood pressure. The results presented here provide a cellular substrate for the clinical use of clonidine as a treatment for hypertension as well as a role in alleviating posttraumatic stress disorder by evoking an increase in parasympathetic cardiac vagal activity, and a decrease in heart rate and blood pressure.

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Recruitment of cardiac parasympathetic activity: effects of clonidine on cardiac vagal motoneurones, pressure lability, and cardiac baroreflex slope in rats

Abstract: Following peripheral beta-blockade, clonidine activated CVMs from a very low baseline, increased the slope of the cardiac baroreflex and sinus arrhythmia, and reduced pressure lability.

Cited by 14 publications

References 48 publications

From Hypertension to Stroke: Mechanisms and Potential Prevention Strategies

From Hypertension to Stroke: Mechanisms and Potential Prevention Strategies

Baroreflex: A New Therapeutic Target in Human Stroke?

Clonidine, an α2-receptor agonist, diminishes GABAergic neurotransmission to cardiac vagal neurons in the nucleus ambiguus

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