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1 University Laboratory of Physiology, Oxford OX1 3PT; 2 Department of Human Anatomy and Genetics, Oxford OX1 3QX, United Kingdom; and 3 Department of Physiology, Monash University, Victoria 3800, Australia
The role of nitric oxide (NO) in the vagal
control of heart rate (HR) is controversial. We investigated the
cholinergic regulation of HR in isolated atrial preparations with an
intact right vagus nerve from wild-type (nNOS+/+, n = 81) and neuronal NO synthase (nNOS) knockout (nNOS
/,
n = 43) mice. nNOS was immunofluorescently colocalized
within choline-acetyltransferase-positive neurons in nNOS+/+ atria. The
rate of decline in HR during vagal nerve stimulation (VNS, 3 and 5 Hz)
was slower in nNOS/ compared with nNOS+/+ atria in vitro
(P < 0.01). There was no difference between the HR
responses to carbamylcholine in nNOS+/+ and nNOS/ atria. Selective
nNOS inhibitors, vinyl-L-niohydrochloride or
1-2-trifluoromethylphenyl imidazole, or the guanylyl cyclase
inhibitor, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one significantly (P < 0.05) attenuated the decrease in HR
with VNS at 3 Hz in nNOS+/+ atria. NOS inhibition had no effect in
nNOS/ atria during VNS. In all atria, the NO donor sodium
nitroprusside significantly enhanced the magnitude of the vagal-induced
bradycardia, showing the downstream intracellular pathways activated by
NO were intact. These results suggest that neuronal NO facilitates vagally induced bradycardia via a presynaptic modulation of neurotransmission.
nitric oxide; parasympathetic; sinoatrial node
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