This Article Full Text Full Text (PDF) All Versions of this Article: 48/6/1137    most recent 01.HYP.0000246493.00385.94v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kamendi, H. Articles by Mendelowitz, D. Search for Related Content PubMed PubMed Citation Articles by Kamendi, H. Articles by Mendelowitz, D. Related Collections Arrythmias-basic studies Other hypertension

(Hypertension. 2006;48:1137.)
© 2006 American Heart Association, Inc.

Original Articles

NO Differentially Regulates Neurotransmission to Premotor Cardiac Vagal Neurons in the Nucleus Ambiguus

Harriet Kamendi; Olga Dergacheva; Xin Wang; Zheng-Gui Huang; Evguenia Bouairi; Christopher Gorini; David Mendelowitz

From the Department of Pharmacology and Physiology, George Washington University, 2300 Eye St, NW, Washington, DC.

Correspondence David Mendelowitz, Department of Pharmacology, George Washington University, 2300 Eye St, NW, Washington, DC 20037. E-mail dmendel{at}gwu.edu

NO is involved in the neural control of heart rate, and NO synthase expressing neurons and terminals have been localized in the nucleus ambiguus where parasympathetic cardiac vagal preganglionic neurons are located; however, little is known about the mechanisms by which NO alters the activity of premotor cardiac vagal neurons. This study examines whether the NO donor sodium nitroprusside ([SNP] 100 µmol/L) and precursor, L-arginine (10 mmol/L), modulate excitatory and inhibitory synaptic neurotransmission to cardiac vagal preganglionic neurons. Glutamatergic, GABAergic, and glycinergic activity to cardiac vagal neurons was examined using whole-cell patch-clamp recordings in an in vitro brain slice preparation in rats. Both SNP, as well as L-arginine, increased the frequency of GABAergic neurotransmission to cardiac vagal preganglionic neurons but decreased the amplitude of GABAergic inhibitory postsynaptic currents. In contrast, both L-arginine and SNP inhibited the frequency of glutamatergic and glycinergic synaptic events in cardiac vagal preganglionic neurons. SNP and L-arginine also decreased glycinergic inhibitory postsynaptic current amplitude, and this response persisted in the presence of tetrodotoxin. Inclusion of the NO synthase inhibitor 7-nitroindazole (100 µmol/L) prevented the L-arginine–evoked responses. These results demonstrate that NO differentially regulates excitatory and inhibitory neurotransmission, facilitating GABAergic and diminishing glutamatergic and glycinergic neurotransmission to cardiac vagal neurons.

Key Words: nitric oxide • parasympathetic • vagal • ambiguus • cardiac • brain stem

This article has been cited by other articles:

				J. Kuncova, J. Sviglerova, W. Kummer, D. Rajdl, M. Chottova-Dvorakova, Z. Tonar, L. Nalos, and M. Stengl Parasympathetic regulation of heart rate in rats after 5/6 nephrectomy is impaired despite functionally intact cardiac vagal innervation Nephrol. Dial. Transplant., August 1, 2009; 24(8): 2362 - 2370. [Abstract] [Full Text] [PDF]

				D. A. Heaton, D. Li, S. C. Almond, T. A. Dawson, L. Wang, K. M. Channon, and D. J. Paterson Gene Transfer of Neuronal Nitric Oxide Synthase into Intracardiac Ganglia Reverses Vagal Impairment in Hypertensive Rats Hypertension, February 1, 2007; 49(2): 380 - 388. [Abstract] [Full Text] [PDF]