TY - JOUR
T1 - The role of neuronal nitric oxide in the vagal control of cardiac interval of the rat heart in vitro
AU - Sweeney, Catherine
AU - Markos, Farouk
PY - 2004/4/30
Y1 - 2004/4/30
N2 - The aim of this study was to examine the role of neuronal nitric oxide (NO) on vagal regulation of the rat heart in vitro using the neuronal nitric oxide synthase (nNOS) inhibitor 1-(2-trifluoromethylphenyl) imidazole (TRIM). All experiments were carried out in the presence of the β-adrenoreceptor antagonist atenolol (4 μM). Right thoracic vagus, or its cardiac branch, was stimulated at frequencies of 2, 4, 8, 16 and 32 Hz (pulse duration 1 ms, 20 V, for 20 s) before and after addition of TRIM (0.14 mM) and cardiac interval (ms) assessed. There was a significant positive linear correlation between cardiac interval and vagal frequency giving a slope of 2.76±0.8 ms/Hz (slope±S.E. slope; data pooled from eight rats) which was significantly attenuated following TRIM to 0.4±0.6 ms/Hz (P<0.05 ANOVA; n=8 rats). Nicotine applied in cumulative concentrations (0.03, 0.1, 0.3, 0.5, 1 mM) caused a linear concentration-dependent increase in cardiac interval, with a slope of 403±72 ms/mM (n=10 rats) which was significantly attenuated after treatment with hexamethonium (28 μM), to 190±36 ms/mM (n=10 rats, P<0.05 ANOVA), and atropine (3 μM) 100±31 ms/mM (n=9 rats, P<0.05 ANOVA) but not following TRIM (0.14 mM) 262±48 ms/mM (n=9 rats, P<0.05 ANOVA). These results suggest that NO facilitates vagal effects on the rat heart in vitro by an action at the pre-ganglionic/post-ganglionic synapse.
AB - The aim of this study was to examine the role of neuronal nitric oxide (NO) on vagal regulation of the rat heart in vitro using the neuronal nitric oxide synthase (nNOS) inhibitor 1-(2-trifluoromethylphenyl) imidazole (TRIM). All experiments were carried out in the presence of the β-adrenoreceptor antagonist atenolol (4 μM). Right thoracic vagus, or its cardiac branch, was stimulated at frequencies of 2, 4, 8, 16 and 32 Hz (pulse duration 1 ms, 20 V, for 20 s) before and after addition of TRIM (0.14 mM) and cardiac interval (ms) assessed. There was a significant positive linear correlation between cardiac interval and vagal frequency giving a slope of 2.76±0.8 ms/Hz (slope±S.E. slope; data pooled from eight rats) which was significantly attenuated following TRIM to 0.4±0.6 ms/Hz (P<0.05 ANOVA; n=8 rats). Nicotine applied in cumulative concentrations (0.03, 0.1, 0.3, 0.5, 1 mM) caused a linear concentration-dependent increase in cardiac interval, with a slope of 403±72 ms/mM (n=10 rats) which was significantly attenuated after treatment with hexamethonium (28 μM), to 190±36 ms/mM (n=10 rats, P<0.05 ANOVA), and atropine (3 μM) 100±31 ms/mM (n=9 rats, P<0.05 ANOVA) but not following TRIM (0.14 mM) 262±48 ms/mM (n=9 rats, P<0.05 ANOVA). These results suggest that NO facilitates vagal effects on the rat heart in vitro by an action at the pre-ganglionic/post-ganglionic synapse.
KW - Nitric oxide
KW - TRIM
KW - Vagus
UR - https://www.scopus.com/pages/publications/2942588991
U2 - 10.1016/j.autneu.2004.04.004
DO - 10.1016/j.autneu.2004.04.004
M3 - Article
C2 - 15182740
AN - SCOPUS:2942588991
SN - 1566-0702
VL - 111
SP - 110
EP - 115
JO - Autonomic Neuroscience: Basic and Clinical
JF - Autonomic Neuroscience: Basic and Clinical
IS - 2
ER -