Abstract:In rats, the nitric oxide (NO)-synthase pathway is present in skeletal muscle, vascular smooth muscle, and motor nerve terminals. Effects of NO were previously studied in rat neuromuscular preparations receiving low (0.2 Hz) or high (200 Hz) frequencies of stimulation. The latter frequency has always induced tetanic fade. However, in these previous studies we did not determine whether NO facilitates or impairs the neuromuscular transmission in preparations indirectly stimulated at frequencies which facilitate … Show more
“…Moreover, Wang et al in 1995 noticed that c.GMP-dependent kinase phosphorylate the nicotinic acetylcholine receptor subunits in cultured myocytes. 16,17,18 .…”
Section: Discussionmentioning
confidence: 99%
“…In addition, Queiroz and Alves -Do-Prado 2001 suggested that, the increase in the amplitude of muscle contraction produced at different frequencies, depend on the metabolism of L-argnine producing additional NO in the tissues and its ability to scavenge superoxide anions. They reported that NOS activity might change according to the applied frequency of stimulation to the motor nerve 3 . It was also possible that during high-frequency stimulation, presynaptic as well as postsynaptic components are activated through a variety of signal transduction cascades.…”
Section: The Effect Of Nitric Oxide On the Rat Diaphragm At Differentmentioning
confidence: 99%
“…Intracellular NO production is catalyzed by several isoforms of an enzyme termed, nitric oxide synthase (NOS). Neural NOsynthase is present in the sarcolemmma of type II skeletal muscle fibers 3 . In rats, the nitric oxide (NO) synthase pathway is present in skeletal muscle, vascular smooth muscle and motor nerve terminal 3,4 .…”
Section: Introductionmentioning
confidence: 99%
“…Neural NOsynthase is present in the sarcolemmma of type II skeletal muscle fibers 3 . In rats, the nitric oxide (NO) synthase pathway is present in skeletal muscle, vascular smooth muscle and motor nerve terminal 3,4 . This study aims to investigate the effect of NO in rat neuromuscular preparation (diaphragm) at different frequencies of nerve stimulation and modulation of its effect by hemoglobin as NO scavenger.…”
Results: In presence of NO Gp1 showed a significant increase in (AMC) (ΔY) and (ΔX) with a significant decrease in (½ Rt). Gp2 showed a significant increase in (AMC)(ΔY).
Conclusion: Nitric oxide (NO) facilitates neuromuscular transmission at presynaptic level. BovineHemoglobin reduces Nitric oxide's induced effects.
“…Moreover, Wang et al in 1995 noticed that c.GMP-dependent kinase phosphorylate the nicotinic acetylcholine receptor subunits in cultured myocytes. 16,17,18 .…”
Section: Discussionmentioning
confidence: 99%
“…In addition, Queiroz and Alves -Do-Prado 2001 suggested that, the increase in the amplitude of muscle contraction produced at different frequencies, depend on the metabolism of L-argnine producing additional NO in the tissues and its ability to scavenge superoxide anions. They reported that NOS activity might change according to the applied frequency of stimulation to the motor nerve 3 . It was also possible that during high-frequency stimulation, presynaptic as well as postsynaptic components are activated through a variety of signal transduction cascades.…”
Section: The Effect Of Nitric Oxide On the Rat Diaphragm At Differentmentioning
confidence: 99%
“…Intracellular NO production is catalyzed by several isoforms of an enzyme termed, nitric oxide synthase (NOS). Neural NOsynthase is present in the sarcolemmma of type II skeletal muscle fibers 3 . In rats, the nitric oxide (NO) synthase pathway is present in skeletal muscle, vascular smooth muscle and motor nerve terminal 3,4 .…”
Section: Introductionmentioning
confidence: 99%
“…Neural NOsynthase is present in the sarcolemmma of type II skeletal muscle fibers 3 . In rats, the nitric oxide (NO) synthase pathway is present in skeletal muscle, vascular smooth muscle and motor nerve terminal 3,4 . This study aims to investigate the effect of NO in rat neuromuscular preparation (diaphragm) at different frequencies of nerve stimulation and modulation of its effect by hemoglobin as NO scavenger.…”
Results: In presence of NO Gp1 showed a significant increase in (AMC) (ΔY) and (ΔX) with a significant decrease in (½ Rt). Gp2 showed a significant increase in (AMC)(ΔY).
Conclusion: Nitric oxide (NO) facilitates neuromuscular transmission at presynaptic level. BovineHemoglobin reduces Nitric oxide's induced effects.
“…In contrast, L-arginine and SIN-1 reduce the maximal tetanic tension (postsynaptic action) when a high stimulation frequency is applied directly to diaphragm preparations previously treated with d-tubocurarine (11). The presynaptic and postsynaptic effects of NO were also observed in assays performed at high frequency with superoxide dismutase, a selective scavenger of superoxide anion radicals (11,12). Since the NO-induced neuromuscular effects may depend on a direct and/or indirect interaction with K + channels, the present study was undertaken to determine the neuromuscular effects of the NO precursor L-arginine and of 8-Br-cGMP on the rat phrenic nerve diaphragm preparation previously treated with a K + channel blocker.…”
Section: -Aminopyridine Inhibits the Neuromuscular Effects Of Nitricmentioning
The effects induced by nitric oxide (NO) in different tissues depend on direct and/or indirect interactions with K + channels. The indirect interaction of NO is produced by activation of guanylyl cyclase which increases the intracellular cGMP. Since NO, cGMP and 4-aminopyridine alone induce tetanic fade and increase amplitude of muscular contractions in isolated rat neuromuscular preparations, the present study was undertaken to determine whether or not the neuromuscular effects of NO and 8-Br-cGMP can be modified by 4-aminopyridine. Using the phrenic nerve and diaphragm muscle isolated from male Wistar rats (200-250 g), we observed that L-arginine (4.7 mM) and 8-Br-cGMP (18 µM), in contrast to D-arginine, induced an increase in the amplitude of muscle contraction (10.5 ± 0.7%, N = 10 and 8.0 ± 0.7%, N = 10) and tetanic fade (15 ± 2.0%, N = 8 and 11.6 ± 1.7%, N = 8) at 0.2 and 50 Hz, respectively. N G -nitro-L-arginine (4 mM, N = 8 and 8 mM, N = 8) antagonized the effects of L-arginine. 4-Aminopyridine (1 and 10 µM) caused a dose-dependent increase in the amplitude of muscle contraction (15 ± 1.8%, N = 9 and 40 ± 3.1%, N = 10) and tetanic fade (17.7 ± 3.3%, N = 8 and 37.4 ± 1.3%, N = 8). 4-Aminopyridine (1 µM, N = 8) did not cause any change in muscle contraction amplitude or tetanic fade of preparations previously paralyzed with d-tubocurarine or stimulated directly. The effects induced by 4-aminopyridine alone were similar to those observed when the drug was administered in combination with L-arginine or 8-Br-cGMP. The data suggest that the blockage of K + channels produced by 4-aminopyridine inhibits the neuromuscular effects induced by NO and 8-Br-cGMP. Therefore, the presynaptic effects induced by NO seem to depend on indirect interactions with K + channels.
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