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PubMed1993

Calcium current inactivation in denervated rat skeletal muscle fibres.

1. The inactivation of the calcium current (ICa) was studied in single extensor digitorum longus muscle fibres of the rat. Denervation was performed by surgically removing 6-8 mm of the sciatic nerve at the sciatic notch. Electrical recordings were carried out using the double Vaseline-gap technique. Normal fibres were used as controls. 2. The time course of the onset of ICa inactivation was studied with double pulse experiments. Denervation after 14 days slowed down the onset of the inactivation process. Two depolarizing pulses with variable interpulse potential were applied. The rate of recovery from ICa inactivation was analysed with long interpulse intervals (9 to 1 s). The time constants for ICa inactivation (tau i) at -90 mV potential were 4.3 and 2.2 in normal and 14 day-denervated fibres respectively. 3. The onset of ICa inactivation was studied with a double pulse protocol with variable duration of the first pulse with constant interval (120 ms) to the second pulse (300 ms). The plot of [ICa (pulse 2)/ICa(pulse 1)]--first pulse duration relationship was fitted with a single exponential equation. The inactivation time constant (tau h) values for normal and denervated fibres were 428 and 619 ms, respectively. 4. The h infinity-Vm relationship for denervated fibres was shifted toward more negative potentials and ICa did not fully inactivate with large prepulses. The h infinity-Vm relationship was fitted with a Boltzmann equation I/Imax = 1 - (A/[1 + (exp ((Vm1/2 - Vm)/kh))]) where Vm is the potential during the conditioning pulse and A is an amplitude factor. In normal fibres, Vm1/2 (mid-point) and kh (slope) values were -28.7 mV and 7.6 mV, respectively. In 14-day-denervated fibres they were -42.2 and 8.6 mV, respectively. 5. A temperature rise from 17 to 27 degrees C greatly increased the inactivation rate of ICa. This effect was similar in control and denervated fibres. The temperature coefficient quotient (Q10) values for ICa amplitude in normal and denervated fibres were 2.4 (n = 8) and 2.3 (n = 8), respectively. The Q10 values for the inactivation time constant (tau h) were 5.14 and 5.25, respectively. ICa decay during 1 s pulses was fitted to a single exponential function in normal fibres at 17 and 27 degrees C; the time constant values were tau h = 460 +/- 53 ms and tau h = 92 +/- 17 ms, respectively. The time constants of denervated fibres at both temperatures were tau h = 644 +/- 102 ms and 146 +/- 17 ms, respectively.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1965

On the differential response of sarcoplasm and myoplasm to denervation in frog muscle.

Electron microscopic evidence is presented that the early response to denervation ("simple atrophy") of the semitendinosus m. of the frog is characterized by a greater prominence of the sarcoplasmic reticulum and by the presence, in the interfibrillar spaces, of mitochondria which are more numerous and smaller than in normal muscle. In contrast with the dynamic changes of the sarcoplasmic structural components, the myofibrils showed a progressive decrease in diameter after denervation and throughout the period studied. By carrying out tissue fractionation experiments, the yield of microsome-protein was found significantly greater in the denervated muscles, as compared with the contralateral controls, in this initial stage. Under the conditions attending the overdevelopment of the sarcoplasmic reticulum (SR), denervated semitendinosus m. incorporated valine-C(14) into proteins more actively than the control pairs. The denervated muscles also showed an increase in the number of freely scattered and membrane-bound ribosomes and of polyribosomes, suggesting a more active synthesis of the SR membranes. Pronounced atrophy of the myofibrils, disorganization of the SR, and an increased number of ribonucleoprotein particles lying in the enlarged interfibrillar spaces were the main ultrastructural features of "degenerative atrophy" in frog muscle in the late periods after denervation. The probably adaptive character of the early changes occurring on denervation of frog muscle is discussed.

Animals↗
PubMed1976

[Pharmacological studies on degeneration and regeneration of peripheral nerves. (1) Effects of methylcobalamin and cobamide on EMG patterns and loss of muscle weight in rats with crushed sciatic nerve].

Experiments were performed to investigate the effects of Vitamin B12, i.e., methylcobalamin and cobamide, on the neural degeneration and regeneration. Male Wistar rats (140 to 150 g) under conditions of experimental unilateral sciatic nerve crushing were treated consecutively with methylcobalamin (50 and 500 mug/kg/day i.p.), cobamide (50 and 500 mug/kg/day i.p.) or saline. EMG recordings were periodically carried out and rats of each group were sacrificed to determine the weight-loss of denervated muscles 1, 2, 3 and 4 weeks after crush. Neither methylcobalamin nor cobamide exerted any significant effect on body-weight gain of the nerve-crushed rats with a daily injection of 50 and 500 mug/kg i.p.. The EMG pattern of the denervated biceps femoris muscle showed a total lack of fibrillation for 2 days after the nerve-crush. Thereafter, the fibrillation appeared and continued for 10 to 14 days until the nerve had regenerated, as evidenced by the appearance of a complex NMU voltage. The occurrence of fibrillation voltage was slightly delayed in methylcobalamin group (500 mug/kg/day) as compared with the saline control group. The re-appearance of normal NMU voltage was more rapid in the methylcobalamin 500 mug/kg group than in controls and other experimental groups. Neither methylcobalamin nor cobamide had any significant effect on the weight-loss of the gastrocnemius and tibialis anterior muscles following crush of the sciatic nerve. However, a daily injection of 500 mug/kg of methylcobalamin produced a significant increase in the weight of the soleus muscle which recovered to the extent of being the same weight of the contralateral 4 weeks after the nerve-crush. These results suggest that methylcobalamin may have an inhibitory effect on Wallerian degeneration and also a facilitatory effect on the neural regeneration of the crushed sciatic nerve of rats.

Animals↗
PubMed1997

A unique myosin isoform transition in cat striated external anal sphincter muscle induced by denervation.

Denervation of limb and trunk muscles leads to characteristic changes in their biochemical properties. However, the effects of denervation of the striated external anal sphincter (EAS) muscle have not been studied, even though denervation is a common etiology for fecal incontinence. The present study reports effects ofdenervation of the cat EAS and compares them with changes in a denervated limb muscle [cat extensor digitorum longus (EDL)]. Nerves supplying the EAS and the EDL were sectioned in anesthetized cats, which were allowed to recover and live for 10, 30, or 60 days. Their muscles were then excised, and myofibrillar proteins were isolated. Myosin heavy chain (MHC) isoform composition was measured by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The EDL and EAS showed progressive increases in MHC type IIA and progressive decreases in MHC type IIB at 10, 30, and 60 days. MHC type I progressively increased in the EDL but showed no change in the EAS. We hypothesize that this distinctive transition is related to the unique embryological origin and function of the EAS.

Anal Canal↗
PubMed1997

Electron microscopic study of long-term denervated rat skeletal muscle.

BACKGROUND: This study describes the ultrastructure of long-term denervated rat extensor digitorum longus and tibialis anterior muscles, with particular emphasis on understanding the cellular basis for the reduced restorative capacity of long-term denervated muscle. METHODS: In 30 male WI/HicksCar rats, the right hindleg was denervated for periods of 1, 2, 4, 5.5, 6, 7, 12, 14, and 18 months before tissues were prepared for electron microscopy. RESULTS: Atrophy of muscle fibers was prominent by the second month post-denervation. At this time, type II fibers showed greater atrophy than type I fibers. At further periods of denervation, atrophy of all fibers was seen; and with increasing times of denervation the muscle fibers became surrounded by dense mats of collagen fibers. Muscle spindles persisted for the duration of this study. At two and four months, satellite cells showed signs of activation, such as elongated cytoplasmic processes and an increased concentration of cytoplasmic organelles. As denervation progressed, activated satellite cells became more widely separated from their associated muscle fibers, and basal lamina material was deposited between the satellite cells and muscle fibers. Some satellite cells broke free from their muscle fibers, and others acted as bridges between two muscle fibers. Evidence was seen of both muscle fiber degeneration and the regeneration of new muscle fibers, often more than one regenerating fiber beneath a single basal lamina. Loose folds of basal lamina were often present around atrophic muscle fibers. As denervation progressed, the morphology of individual muscle fibers varied. Some contained well-ordered lattice arrays of myofilaments, whereas in others considerable sarcomeric disorganization was evident. Mitochondria became smaller and rounded; elements of the sarcoplasmic reticulum proliferated and became more disorganized; lipid droplets, glycogen deposits, and autophagic vesicles were all present in the cytoplasm of atrophic muscle fibers. CONCLUSIONS: In addition to muscle fiber atrophy, long-term denervated muscles show evidence of myofiber and capillary death, as well as the deposition of massive amounts of interstitial collagen. These changes, all of which would appear to reduce the restorative capacity of the denervated muscle, take place concurrently with the morphological activation of satellite cells. The latter indicates that even in the denervated condition, restorative processes occur concurrently with regressive processes.

Animals↗
PubMed1993

[Effect of the mutation muscular dysgenesis on the mitochondrial metabolism of fibroblasts in vitro].

Muscular dysgenesis is a lethal mutation characterized by an absence of striated muscle contraction. This abnormality of function caused by a defect in excitation-contraction coupling is due to the lack of the alpha 1 subunit from the dihydropyridine receptor in the transverse tubule membrane. A phenotypical reversion is obtained in vitro by addition of normal cells, as fibroblasts, in dysgenic muscle culture. Perisynaptic fibroblasts from denervated muscle have been shown to synthetize molecules which are usually concentrated at the synapses suggesting that signal arising after denervation may influence fibroblasts synthesis ability. We show here that the energetic metabolism level from dysgenic fibroblast is lower than that from normal fibroblasts. The synthesis or the release of muscular signals that are involved in fibroblast differentiation could be disturbed in mdg/mdg myotubes.

Electron Transport↗
PubMed1993

Expression of myogenic factors in denervated chicken breast muscle: isolation of the chicken Myf5 gene.

In this study, we have isolated and characterized the chicken Myf5 gene, and cDNA clones encoding chicken MyoD1 and myogenin. The chicken Myf5 and MRF4 genes are tandemly located on a single genomic DNA fragment, and the chicken Myf5 gene is organized into at least three exons. Using genomic and cDNA probes, we further analyzed the mRNA levels of four myogenic factors during chicken breast muscle development. This analysis revealed that myogenin expression is restricted to in ovo stages in breast muscle, and is not detectable in neonatal and adult stages. On the other hand, Myf5 expression is detectable until day 7 post-hatching, and is not found in adult muscle, whereas high levels of MyoD1 and MRF4 are detectable at all stages. To further understand the roles of innervation on muscle maturation, we analyzed the expression of the four myogenic factors in denervated adult breast muscle. We found that MyoD1, myogenin, and MRF4 are induced at high levels in denervated muscle, whereas no change occurs in the level of Myf5. These studies suggest that innervation controls the relative abundance and type of myogenic factors that are expressed in adult muscle, and that when nerve control is removed, the muscle reverts to a neonatal phenotype, with the enhanced expression of three myogenic factors (MyoD1, myogenin, and MRF4).

Amino Acid Sequence↗
PubMedDate not supplied

Immunolocalization of tenascin-C in human type II fiber atrophy.

Tenascin-C is a multifunctional extracellular matrix glycoprotein with stimulatory and anti-adhesive or inhibitory properties for axon growth. Its location and discontinuous expression are restricted in innervated muscle tissues. Tenascin-C accumulated interstitially among human denervated muscle fibers and close to normal-sized fibers. To expand our knowledge of the expression of tenascin-C in human neuromuscular disorders, we investigated immunohistologically 20 human muscle specimens with type II myofiber atrophy of children and adults. Tenascin-C immunoreactivity in adult type II atrophy was frequent, and accumulation in children was sparse and weak. In both groups, tenascin-C immunoreactivity was found: 1. Interstitially around normal-sized type II muscle fibers. 2. Around atrophic type II muscle fibers. 3. Around small-caliber myofibers with centrally located nuclei. These results indicate that tenascin-C immunoreactivity: (1) is detectable around early denervated and reinnervated muscle fibers and, therefore, (2) may reflect in part the molecularly ongoing process of denervation and reinnervation in human type II fiber atrophy.

Adult↗
PubMed1987

Dynamics of insulin resistance in denervated slow and fast muscles in vivo.

Sciatic nerve in one hindlimb of rats was sectioned, and animals were investigated 3, 6, 9, and 24 h and 3, 8, and 17 days after surgery. Cellular uptakes of 2-deoxy-D-glucose (DG) and alpha-aminoisobutyric acid (AIB) by soleus, plantaris, and gastrocnemius muscles of the denervated and contralateral sham hindlimb were compared in vivo. Effects of insulin on DG and AIB uptakes by soleus and plantaris muscles, but not gastrocnemius muscles, were reduced 20-58% as early as 3-6 h after denervation. Three to 17 days after denervation, soleus muscle did not respond to insulin stimulation of DG uptake, whereas plantaris and gastrocnemius muscles responded, but the insulin-induced increment in DG uptake was reduced 24-68% compared with the sham muscles. In contrast, none of the denervated muscles increased AIB uptake in response to insulin stimulation 3-17 days after surgery. The levels of creatine phosphate and ATP in calf muscles frozen in situ 3 days after denervation were increased 7 and 9%, respectively, and those of ADP, AMP, glucose-6-phosphate, and lactate were unchanged compared with sham muscles. It is concluded that muscle denervation results in a rapid development of insulin resistance, the effect of denervation depends on muscle fiber population, and insulin resistance of denervated muscles is not due to a cellular energy deficit.

Aminoisobutyric Acids↗
PubMed1974

The formation of synapses in reinnervated and cross-reinnervated striated muscle during development.

1. A study has been made of the formation of synapses in reinnervated and cross-reinnervated developing striated muscles which normally receive either a focal or distributed innervation, using histological, ultrastructural and electrophysiological techniques.2. The focally innervated mammalian tibialis anterior muscle, denervated soon after birth, was reinnervated at both the original end-plates as well as on the new muscle added during the period of denervation; but not on the muscle present at the time of denervation. Nearly all the synapses which had formed, other than at the original end-plates, disappeared by 6 weeks post-natal.3. The avian anterior latissimus dorsi muscle (ALD), which receives a distributed innervation, was denervated during the first week post-hatched, and became reinnervated both at the original synaptic sites as well as on the new muscle added during the period of denervation; all these synapses were spaced approximately 200 mum apart along the length of individual muscle cells.4. The myofibres of the ALD muscle cross-reinnervated at hatching with the superior brachialis nerve, which contains fast motor axons that normally form a focal innervation, were each focally innervated by a single ;en plaque' terminal; these synapses had the same electrical properties as normal synapses formed by fast motor axons.5. Many of the myofibres of the avian posterior latissimus dorsi (PLD), which normally receive a focal innervation, received a distributed innervation from ;en grappe' terminals when cross-reinnervated with the ALD nerve at hatching.6. It is suggested that during development the nerve type determines the pattern of synapses over an effector; this is achieved by the nerve, after forming the initial synaptic contact, making the rest of the muscle cell membrane refractory to further synapse formation for some distance, this distance being determined by the nerve type.

Action Potentials↗
PubMed1992

Synaptic basal lamina contains a signal for synapse-specific transcription.

Nuclei in the synaptic region of multinucleated skeletal myofibers are transcriptionally distinct, since acetylcholine receptor genes are transcribed at a high rate by these nuclei, but not by nuclei elsewhere in the myofiber. Although this spatially restricted transcription pattern is presumably imposed by the motor nerve, the continuous presence of the nerve is not required, since synapse-specific transcription persists after denervation. These results suggest either that a transcriptional signal persists at synaptic sites after nerve terminals have degenerated, or that a transcriptional pattern in the myofiber, once established, is stable in the absence of a nerve-derived signal. To distinguish between these possibilities, we denervated muscle and damaged the myofibers and specialized cells located near synaptic sites, and then studied transcription of an acetylcholine receptor gene in myofibers that regenerated in their original basal lamina sheaths, but remained denervated. We show that synapse-specific transcription is re-induced in these regenerated myofibers, and we conclude that a signal for synapse-specific transcription is stably maintained in the synaptic basal lamina.

Animals↗
PubMed1992

Effects of denervation on laryngeal muscles: a canine model.

The purpose of this study was to chronologically evaluate the changes in functional and histomorphometry of denervated laryngeal muscles. In 14 adult mongrel dogs, a 2.5-cm segment of the right recurrent laryngeal nerve was excised. Videolaryngoscopy and electromyography were performed at 1, 2, 3, 4, 5, 6, and 9 months under intravenous sedation. The animals were then killed, and the laryngeal muscles were processed for histochemical reactions. The mean muscle fiber diameter, standard deviation, and muscle fiber type composition were determined. The findings indicate that, following recurrent laryngeal nerve sectioning, the canine intrinsic laryngeal muscles undergo denervation atrophy for approximately 3 months, after which reinnervation occurs. The source of reinnervation appears to be from regenerated nerve fibers of the sectioned recurrent laryngeal nerve. The nerve fibers nonselectively reinnervated the abductor and adductor muscles of the larynx.

Action Potentials↗
PubMed1977

Appearance of new acetylcholine receptors on the baby chick biventer cervicis and denervated rat diaphragm muscles after blockade with alpha-bungarotoxin.

1. The recovery of contractile responses and appearance of new alpha-bungarotoxin-binding sites were studied in the baby chick biventer cervicis and the rat diaphragm muscles after saturating the existing acetylcholine (ACh) receptors (AChR) with alpha-bungarotoxin in vitro.2. Washout of alpha-bungarotoxin restored gradually the response to exogenous ACh attaining about 30% recovery in 3 hr either in the chick muscle or in the denervated rat diaphragm. No recovery was obtained, however, for the response to nerve stimulation.3. The recovery of ACh-response was abolished by decreasing the bath temperature to 9 degrees C during the washout of the toxin whereas the recovery was not reduced in the presence of cycloheximide.4. The half-life of [(3)H]acetyl alpha-bungarotoxin bound specifically on the existing AChRs, junctional and extrajunctional receptors combined, was 16 hr in the chick muscle. That on the extrajunctional AChR was estimated to be 8 hr.5. New toxin-binding sites were found to be incorporated on the membrane of extrajunctional site rapidly after treatment with alpha-bungarotoxin in the chick and the denervated rat muscles along the muscle fibres but not in the innervated rat diaphragm. Treatment with (+)-tubocurarine, ACh or decamethonium did not cause an appreciable increase of the toxin-binding sites.6. The appearance of new binding sites was progressive during 5 hr at a rate of 24 sites/mum(2).hr in the chick muscle and 42 sites/mum(2).hr in the rat diaphragm denervated for 7 days. The existing extrajunctional AChR were about 50/mum(2) and 192/mum(2), respectively.7. ACh effectively antagonized the binding of alpha-bungarotoxin with the new sites whereas (+)-tubocurarine was less effective than its effect on the existing AChR.8. The new toxin-binding sites appeared to have a reduced capacity to evoke ACh response.9. The incorporation of new binding sites was reduced by lowering of the temperature, treatment with dinitrophenol, high K(+), high Ca(2+) and by the stimulation of either nerve or muscle. Cycloheximide, ACh, decrease of [Na(+)](o) and increase of [Mg(2+)](o) were without effect.10. It is suggested that binding of the extrajunctional AChRs with alpha-bungarotoxin cause a change of membrane architecture and trigger the incorporation of cytoplasmic AChR-precursor or hidden AChR into the membrane.

Acetylcholine↗
PubMed1976

[Muscle spindles in denervated and reinnervated m. soleus of the rat. I. Changes in number, distribution and length of muscle spindles].

After a transient or permanent unilateral denervation of the soleus muscle of the rat the number, distribution and length of muscle spindles were determined. The results were compared with those of the contralateral innervated muscle and with the data received from investigating soleus muscles of normal uninjured rats. Denervation (with or without reinnervation) reduces the number of muscle spindles by nearly 50%. The typical uniform distribution of muscle spindles in the muscle remains almost unchanged. The remaining muscle spindles grow longer. The same findings are observed in the contralateral still innervated muscles, too. Consequently a comparison of the denervated (reinnervated) muscle exclusively with its contralateral muscle does not show different counts of muscle spindles. Therefore in such investigations the contralateral muscle is of dubious value as a mean of control. As regards number, distribution and length of muscle spindles there exist only small differences between the various strains of rats.

Animals↗
PubMed1984

Reanimation of the hemiparalytic tongue.

Tongue hemiparesis is the inevitable result when the freshly severed 12th nerve is anastomosed to the trunk of a paralyzed 7th nerve in the technique commonly used by neurosurgeons, head and neck surgeons, otologists, and plastic surgeons to treat unilateral facial paralysis. This author has reactivated hemiparalytic tongues after research on cats. The technique has now been proved to be successful on two human beings. The reanimation is based on a simple Z-plasty of tongue muscle across the midline. Two principles are established: (1) placing a normal muscle in direct contact with a denervated muscle stimulates axons from the normal side to penetrate into the denervated side, eventually restoring function, and (2) transposition of a flap of muscle from the normal side containing extrinsic tongue muscles could provide a motor apparatus to activate the paralytic side. Biopsy slides taken from the paralyzed side of the cat tongues after 18 months showed sprouting of multiple nerves. Nerve sprouting can be found in human tongues 1 year after Z-plasties. The two patients who experienced atrophy and hemiparesis after the 12th-7th nerve hookup regained full range of tongue movements by 2 months and 4 months, respectively, demonstrating that with time, motor axons from the normal side innervated the atrophic muscle side to form new neuromotor junctions resulting in tongue movements. EMGs of the reanimated tongue showed normal activity in both sides of the tongue. Biopsies of the interface between the normal and former paralyzed side taken 1 year later showed nerves crossing the scar barrier. Apparently, the role of additional extrinsic muscle to the paralyzed side played a minor role.

Animals↗
PubMed1989

Passive exercise and reinnervation of the rat denervated extensor digitorum longus muscle after nerve crush.

Denervated extensor digitorum longus muscles of Wistar rats were passively exercised for 4 days (2 h/day) after peroneal nerve crush 1 cm from the muscle. Isometric contractile properties and endplate ultrastructure were measured 11 days postcrush. No significant differences were observed in tension characteristics between the exercised and nonexercised muscles on day 11. However, the postsynaptic area of endplates for exercised muscles were closer in size to controls than those for the nonexercised ones. In addition, the endplates from the exercised muscles exhibited increased numbers of axonal sprouts and terminals than nonexercised muscles. These results demonstrate that denervated muscles exercised 4 days before reinnervation can preserve the structure of the endplate as well as enhance reinnervation and sprouting at these endplates after 11 days of denervation.

Animals↗
PubMed1969

Some properties of the denervated anterior gracilis muscle of the rat.

1. Microdrops of acetylcholine (ACh) were topically applied to denervated, mammalian skeletal muscle in vivo, and ACh-evoked depolarization and contracture were recorded simultaneously.2. Contracture tension was directly proportional to the degree of ACh-elicited depolarization.3. Atropine and (+)-tubocurarine increased the amount of ACh required to produce a given amount of depolarization, but these anticholinergic agents did not alter the relationship between the degree of ACh-evoked depolarization and contracture tension.4. Topically applied catecholamines did not produce either depolarization or contracture, despite the fact that parenterally administered catecholamines elicited both responses.

Acetylcholine↗
PubMed1992

Influence of denervation on smooth muscle response to repeated administration of cyclophosphamide, cytosine arabinoside, or their combination.

Cyclophosphamide, 40 mg.kg-1, cytosine arabinoside, 2 mg.kg-1 or their combination, were all given once weekly to chicks for 5 weeks. The expansor secundariorum muscle of the left wing of each chick was then surgically denervated leaving that of the right wing to serve as the control. Drug administrations continued for a further 5 weeks before the responses of normal and denervated expansor muscles were determined pharmacologically. Cyclophosphamide depressed the response of the expansor muscle to noradrenergic nerve stimulation but enhanced the response to noradrenaline and potassium chloride. Cytosine arabinoside enhanced responses of expansor muscles to noradrenergic nerve stimulation and noradrenaline, but depressed responses evoked by potassium chloride. The combination enhanced responses to nerve stimulation, noradrenaline, and potassium chloride. Expansor muscles were unresponsive to acetylcholine and anticancer drugs failed to restore the responsiveness to acetylcholine except the combination. Denervation depressed responses to noradrenergic nerve stimulation but caused supersensitivity to noradrenaline; this was more marked in the combination and cyclophosphamide groups, with no change in sensitivity seen in the cytosine arabinoside group. The denervated expansor muscle responded to acetylcholine in the order, combination much greater than cyclophosphamide greater than control greater than cytosine group. Denervated expansor muscles from anticancer groups were supersensitive to potassium chloride, with the combination group having the most pronounced effect. It is suggested that denervation influences smooth muscle sensitivity to agonist drugs which can modify the effects of anticancer drugs on smooth muscle.

Adrenergic Fibers↗