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University Laboratory of Physiology, Oxford OX1 3PT, United Kingdom
The role of the
cardiac muscarinic-receptor-coupled nitric oxide (NO) pathway in the
cholinergic control of heart rate (HR) is controversial. We
investigated whether adding excessive NO or its intracellular messenger
cGMP could significantly modulate the HR response to vagal nerve
stimulation (VNS) in the anesthetized rabbit and isolated guinea pig
atria. The NO donor molsidomine (0.2 mg/kg iv) significantly enhanced
the decrease in HR seen with right VNS (5 Hz, 5 V, 30 s) in vivo. A
qualitatively similar effect was seen with the NO donor sodium
nitroprusside (SNP; 10 and 100 µM) during VNS in vitro. This effect
was still present when the baseline shift in HR caused by SNP was
eliminated by using the specific hyperpolarization-activated current
antagonist 4-(N-ethyl-N-phenylamino)-1,2-dimethyl-6-(methylamino)-pyrimidinium chloride (ZD-7288, 1 µM). The accentuated decrease in HR
with SNP during VNS was mimicked by the stable analog of cyclic GMP, 8-bromoguanosine 3',5'-cyclic monophosphate (0.5 mM). This,
however, was not seen with bath application of the stable analog of
acetylcholine, carbamylcholine chloride (100 nM). We conclude that
excessive NO enhances the magnitude of the decrease in HR caused by
VNS. This effect appears to involve a presynaptic action via a
cGMP-dependent pathway because it was not mimicked by bath-applied
carbamylcholine chloride.
nitric oxide; vagal; heart rate; guanosine 3',5'-cyclic monophosphate
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