Atropine and ODQ antagonize tetanic fade induced by L-arginine in cats

Cruciol, Joice Mara; Alves-Do-Prado, Wilson

doi:10.1590/s0100-879x1999001000015

Cited by 2 publications

(3 citation statements)

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“…In cats it has been shown that tetanic fade induced by NO depends on the action of gas at the presynaptic level; it might increase acetylcholine release from motor nerve terminals, with a consequent activation of inhibitory presynaptic muscarinic receptors (15). Such mechanism might explain the reduction in R values obtained with NO at 50 Hz, but not the increase in R values recorded with NO at 5 Hz.…”

mentioning

confidence: 94%

Effects of L-arginine on the diaphragm muscle twitches elicited at different frequencies of nerve stimulation

Queiroz

Alves-Do-Prado

2001

Braz J Med Biol Res

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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 neuromuscular transmission. Thus, the present study was carried out to examine the effects of NO in rat neuromuscular preparations indirectly stimulated at 5 and 50 Hz. The amplitude of muscular contraction observed at the end (B) of a 10-s stimulation was taken as the ratio (R) of that obtained at the start (A) (R = B/A). S-nitroso-N-acetylpenicillamine (200 µM), superoxide dismutase (78 U/ml) and L-arginine (4.7 mM), but not D-arginine (4.7-9.4 mM), produced an increase in R (facilitation of neurotransmission) at 5 Hz. However, reduction in the R value (fade of transmission) was observed at 50 Hz. N G -nitro-L-arginine (8.0 mM) antagonized both the facilitatory and inhibitory effects of L-arginine (4.7 mM). The results suggest that NO may modulate the release of acetylcholine by motor nerve terminals. Key words Nitric oxide (NO) is synthesized by NOsynthase (NOS) (1-3). In the rat, NOS is present in the sarcolemma of type II fibers of skeletal muscle (4), in vascular smooth muscle (5), and in motor nerve terminals (6). Since NOS is a stereospecific enzyme, the effects induced by L-arginine are not observed in the presence of D-arginine under similar experimental conditions (7,8)L-arginine methyl ester; L-arginine ethyl ester, and N G -nitro-L-arginine methyl ester) are used as inhibitors of NOS. The effects produced by endogenous NO (from L-arginine) are pharmacologically similar to those induced by NO released from an exogenous source such as 3-(4-morpholinyl)-syndonone imine (SIN-1) or S-nitroso-N-acetylpenicillamine (SNAP) (9).The amplitude of muscular contraction (AMC) is stable when the diaphragm is indirectly stimulated at 0.2 Hz. A progressive increase in AMC is observed at 5 Hz (see Acting at the presynaptic level, the NO precursor L-arginine (4.7-9.4 mM) produces a dose-dependent increase of AMC in rat neuromuscular preparations indirectly stimulated at 0.2 Hz (10). In contrast, acting on skeletal muscle, it reduces AMC in preparations previously paralyzed with d-tubocurarine and directly stimulated at 0.2 Hz (10). The presynaptic action of NO reduces the effect produced by its postsynaptic action (10). On the other hand, the NO precursor Larginine (4.7 to 9.4 mM) or SIN-1 acting at the presynaptic level produces a dose-dependent increase in tetanic fade when the nerve is stimulated at 200 Hz (11). The same high frequency of stimulation reduces the maximal tetanic tension (postsynaptic action) when applied to the rat phrenic nerve diaphragm preparation previously treated with L-arginine o...

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confidence: 94%

Effects of L-arginine on the diaphragm muscle twitches elicited at different frequencies of nerve stimulation

Queiroz

Alves-Do-Prado

2001

Braz J Med Biol Res

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“…This suggests that the effects of NO are mediated by activation of guanylyl cyclase. This hypothesis is supported by results from similar studies showing that ODQ, a guanylyl cyclase blocker, antagonizes the effects induced by NO in neuromuscular preparations of cats or rats (11,14).…”

Section: -Aminopyridine Inhibits the Neuromuscular Effects Of Nitricmentioning

confidence: 53%

“…These effects had their origin at the presynaptic level, as previously shown in 8 9 0 1 2 3 4 5 6 7 8 9 0 1 2 3 4 5 6 7 8 9 0 1 2 3 4 5 6 7 8 9 0 1 2 3 4 5 6 7 8 9 0 1 2 3 4 5 6 7 8 9 0 1 2 3 4 5 6 7 8 9 0 1 2 3 4 5 6 7 8 9 0 1 2 3 4 5 6 7 8 9 0 1 2 3 4 5 6 7 8 9 0 1 2 3 4 5 6 7 8 9 0 1 2 3 4 5 6 7 8 9 0 1 2 3 4 5 6 7 8 9 0 1 2 3 4 5 6 7 8 9 0 1 2 3 4 5 1 2 3 4 5 1 2 3 4 5 1 2 3 4 5 1 2 3 4 5 1 2 3 4 5 1 2 3 4 5 1 2 3 4 5 % 50 0 -25 25 -50 1 2 3 4 5 1 2 3 4 5 1 2 3 4 5 1 2 3 4 5 1 2 3 4 5 1 2 3 4 5 1 2 3 4 5 1 2 3 4 5 1 Figure 2). Therefore, we propose that the effects of L-arginine depend on its metabolism by NOS to produce NO, thereby acting on motor nerve endings (14). Furthermore, current research shows that 8-Br-cGMP (18 µM) induced effects similar to L-arginine ( Figure 2).…”

Section: -Aminopyridine Inhibits the Neuromuscular Effects Of Nitricmentioning

confidence: 66%

4-Aminopyridine inhibits the neuromuscular effects of nitric oxide and 8-Br-cGMP

Queiroz

Ramos

Alves-Do-Prado

2003

Braz J Med Biol Res

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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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Atropine and ODQ antagonize tetanic fade induced by L-arginine in cats

Cited by 2 publications

References 18 publications

Effects of L-arginine on the diaphragm muscle twitches elicited at different frequencies of nerve stimulation

Effects of L-arginine on the diaphragm muscle twitches elicited at different frequencies of nerve stimulation

4-Aminopyridine inhibits the neuromuscular effects of nitric oxide and 8-Br-cGMP

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