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PubMed1983

Alteration of sarcoplasmic reticulum after denervation of chicken pectoralis muscle.

To determine the neural influence on the function of the sarcoplasmic reticulum (SR) of fast-twitch skeletal muscle, the superior pectoralis muscle of adult chicken was denervated, and the SR was isolated at 20 days post-denervation. The isolated SR was probably derived from the longitudinal SR and was relatively free of contaminants. The protein profile of the SR was quantitatively changed after denervation with an increase in the M55 and 30000-mol.wt. proteins relative to the Ca2+-ATPase. Ca2+-dependent ATPase activity and phosphoenzyme formation were lower in the denervated-muscle SR; however, the enzyme catalytic-centre activity was similar to the control value. The decrease in Ca2+-ATPase activity in denervated-muscle SR was accompanied by a lower Ca2+ accumulation so that the relationship between Ca2+ accumulation and Ca2+-dependent ATPase activity was well maintained in the SR from denervated muscle. The data imply that denervation may result in a diminution of functional Ca2+ pump sites. Evidence is presented, though, which suggests that denervation affects a single class of Ca2+-binding sites of the Ca2+-ATPase, resulting in a lower affinity for Ca2+.

Adenosine Triphosphatases↗
PubMed1999

Electrical activity of the corpus cavernosum in denervated rats.

BACKGROUND: We evaluated the electrical activity of the corpus cavernosum after intracavernous papaverine injection in rats that had been denervated experimentally. METHODS: Twenty-four male adult Sprague Dawley rats were divided into three groups: (i) controls (n=8) (ii) unilateral cavernous nerve resection on the right side (n=8); and (iii) bilateral cavernous nerve resection (n=8). Through a suprapubic incision, the urinary bladder was retracted laterally to locate the major pelvic plexus on the lateral surface of the prostate. The major branch of the cavernous nerve, running caudally from the pelvic plexus, was isolated and excised using an operating microscope. Three weeks later, recording of the electrical activity of the corpus cavernosum (EACC) was performed by using a Neuropack-2 EMG unit (Nihon Kohden, Tokyo, Japan) and coencentric needle electrode. Changes in amplitude were evaluated before and after intracavernosal papaverine injection. The results in the flaccid state and after papaverine injection were compared by using the Mann Whitney U-test in all three groups and paired t-test between groups. RESULTS: In the flaccid penis, the mean (+/- SD) amplitude of electrical activity of the corpus cavernosum was 17.42+/-2.05, 12.42+/-1.88, 9.71+/-1.59 and 5.85+/-0.96 microV in control rats, in unilaterally denervated rats (in which the cavernous nerve was intact on the left side), in unilaterally denervated rats in which the cavernous nerve was resected on the right side and in bilaterally denervated rats, respectively. In the flaccid state, EACC is lower in the bilaterally denervated group than in the control and unilaterally nerve-resected groups (P < or = 0.05). The recording of electrical activity of the corpus cavernosum was continued for 20 min after papaverine injection. In the control group and in both groups of unilaterally denervated rats, we observed a significant decrease in the electrical activity of the corpus cavernosum in the first 5 min after papaverine injection (P < or = 0.05). However, no difference was observed in bilaterally denervated rats after injection (P > or = 0.05). CONCLUSIONS: We conclude that electrical activity of the corpus cavernosum continues after unilateral nerve injury in rats. Cross-innervation may play a role in penile innervation and corpus cavernosum electromyography shows electrical activity in denervated rats.

Animals↗
PubMed1999

[Treatment of therapy refractory epicondylitis lateralis humeri by denervation. On the pathogenesis].

PURPOSE: The pathogenesis of tennis elbow is still debated, the question of proper surgical treatment as well. Because the area of pain in tennis elbow and the concomitant spots of pain together with sensibility disorders of the hand are supplied entirely by branches of the radial nerve, we suggested a surgical procedure for complete denervation as early as 1962. The main purpose of this paper is to examine the possibilities of improving the surgical technique, thereby shedding light on the pathogenesis of tennis elbow. METHOD AND MATERIAL: Between 1970 and 1994, altogether 166 patients with 172 cases of resistant tennis elbow were treated by denervation. This procedure calls for careful exposure and the severing of only one tiny branch of the radial nerve. Denervation is otherwise accomplished by "blind" dissection by desinsertion of certain muscles, which are reinserted after denervation, however, with exception of the supinator muscle. Until 1990, the original procedure was performed 39 times (Group A). Afterwards, denervation involved only isolated desinsertion of the supinator muscle in 46 cases (Group B) without the temporary incision of the ECRB-origin, as performed previously. In a further series of 87 cases, an evaluation of denervation in combination with a direct decompression of the deep branch of the radial nerve was performed by resection of the supinator arcade (Group C). Postoperative results were evaluated and scored according to Roles and Maudsley (1972). RESULTS: The denervations of Group A were controlled after an average follow-up time of 9.7 years in 36 cases (92.3%), in 91.6% they demonstrated good and excellent results. In Group B, 42 patients (91.3%) were followed-up after an average time of 4.9 years; these cases showed about the same results as in Group A (90.5% good and excellent). The time off work was 2.7 and 5.7 weeks respectively. The results of denervation, however, were not improved by additional direct decompression of the posterior interosseous nerve (Group C); in a follow-up rate of 86% after 3.6 years only 65.3% showed good and excellent results together with an extremely long time off work of up to 11.7 weeks. CONCLUSION: The results in Group A and B prove that the temporary desinsertion of the ECRB, previously regarded as necessary for reasons of dissection, can be discontinued, without worsening of outcome, as long as the anterior and lateral portions of the supinator origin are incised directly, thereby resulting in indirect decompression of the posterior interosseous nerve simultaneously. The results of this procedure emphasize the fact that tennis elbow is the result of a compression syndrome of the radial nerve and its branches, where the pain-triggering nerve irritations are found at one or several localizations that can be treated successfully--as shown in the literature and by our own findings--by direct decompression of this nerve segment.

Adult↗
PubMed1997

Exercise training of moderate intensity does not abate the effects of denervation on muscle morphology.

Denervation elicits profound alterations in the morphometry of skeletal muscle. These alterations include changes in fiber type composition as well as reductions in fiber size. There is evidence that the increased mechanical load placed upon muscle via rhythmic stretching attenuates denervation induced alterations in muscle morphology. The purpose of the present study was to determine whether the mechanical stimuli associated with exercise training, i.e. rhythmic stretching and mechanical loading, would effectively moderate the changes in muscle morphometry observed following denervation. Unilateral denervation of the soleus muscle of eight male Sprague-Dawley rats was performed under aseptic conditions. The animals were then randomly assigned to two groups: sedentary controls and exercise trained. The exercise training protocol featured treadmill running five days per week for six weeks. At the conclusion of the experimental period, animals from both groups were sacrificed and soleus muscles were histochemically analyzed for muscle morphometry. Results demonstrated that denervation caused marked alterations in fiber type profile and in fiber cross-sectional areas. Interestingly, the degree of denervation induced atrophy appeared to be fiber type specific. However, the data presented here indicate that in denervated soleus muscles there were no significant differences in fiber type composition or fiber size between the sedentary and exercise trained groups. Hence, it appears that the mechanical stimuli provided by treadmill running of moderate intensity and duration are not sufficiently potent to ameliorate muscle morphometric responses to denervation.

Animals↗
PubMed2002

Effects of extrinsic autonomic denervation and myenteric plexus transection on colonic motility in conscious dogs.

BACKGROUND: The role of extrinsic autonomic nerves in regulation of colonic contractile activity is not well understood. METHODS: Twelve dogs had 6 strain gauge force transducers implanted in the colon and were divided into 3 experimental groups: (1) a control group, (2) an extrinsic denervation group (denervation group), and (3) an extrinsic denervation with proximal intrinsic myenteric plexus transection group (denervation + transection group). After recovery, colonic contractile activity during fasting and effects of feeding on gastrocolonic response were recorded. RESULTS: Colonic contractile activity occurred not only in the denervation group but also in the denervation + transection group. Both mean duration and propagation time of the colonic contractile activity were shorter in the denervation + transection group than in the control group. In the denervation group, propagation time was shorter than in the controls but the other parameters were not different. Feeding failed to immediately induce the gastrocolonic response in both experimental groups. CONCLUSIONS: We conclude that extrinsic nerves are not required for the appearance of colonic contractile activity. However, colonic contractile activity and its propagation are modulated by extrinsic innervation or proximal intrinsic neural continuity. Gastrocolonic response may be predominantly under extrinsic neural control.

Animals↗
PubMed1984

Denervated skeletal muscle displays discoordinate regulation for the synthesis of several myofibrillar proteins.

Synthesis patterns of myosin heavy- and light-chain isoforms, tropomyosin and troponin, have been studied in chicken fast muscle denervated at both neonatal and adult stages. Denervated neonatal muscle does not synthesize the adult myosin heavy-chain isoform at the time of denervation, but it does synthesize the adult isoform several months after denervation. Thus, innervation does not appear to be necessary for the normal sequential replacement of embryonic and neonatal myosin heavy chain by the adult variant. Nerve is required, however, for the regulation of tropomyosin and troponin expression. Normally the pectoralis major muscle represses synthesis of both beta-tropomyosin and leg-type troponin T during late embryonic development. After denervation, however, the muscle relaxes its ongoing repression of these proteins and significant amounts of both beta-tropomyosin and leg-type troponin T are synthesized by the muscle. Denervation also results in an altered pattern of myosin light-chain synthesis so that the ratio of fast light-chain 3/fast light-chain 1 decreases. Similar results are found in muscle denervated at the adult stage. In denervated muscle, therefore, synthesis of these myofibrillar proteins is not coordinated: ongoing isoform shifts proceed to express an adult pattern of myosin heavy chain while tropomyosin, troponin, and myosin light-chain patterns appear to revert to embryonic configurations.

Aging↗
PubMed1989

Fibroblasts that proliferate near denervated synaptic sites in skeletal muscle synthesize the adhesive molecules tenascin(J1), N-CAM, fibronectin, and a heparan sulfate proteoglycan.

Four adhesive molecules, tenascin(J1), N-CAM, fibronectin, and a heparan sulfate proteoglycan, accumulate in interstitial spaces near synaptic sites after denervation of rat skeletal muscle (Sanes, J. R., M. Schachner, and J. Covault. 1986. J. Cell Biol. 102:420-431). We have now asked which cells synthesize these molecules, and how this synthesis is regulated. Electron microscopy revealed that mononucleated cells selectively accumulate in perisynaptic interstitial spaces beginning 2 d after denervation. These cells were identified as fibroblasts by ultrastructural and immunohistochemical criteria; [3H]thymidine autoradiography revealed that their accumulation results from local proliferation. Electron microscopic immunohistochemistry demonstrated that N-CAM is associated with the surface of the fibroblasts, while tenascin(J1) is associated with collagen fibers that abut fibroblasts. Using immunofluorescence and immunoprecipitation methods, we found that fibroblasts isolated from perisynaptic regions of denervated muscle synthesize N-CAM, tenascin(J1), fibronectin, and a heparan sulfate proteoglycan in vitro. Thus, fibroblasts that selectively proliferate in interstitial spaces near synaptic sites are likely to be the cellular source of the interstitial deposits of adhesive molecules in denervated muscle. To elucidate factors that might regulate the accumulation of these molecules in vivo, we analyzed the expression of tenascin(J1) and fibronectin by cultured fibroblasts. Fibroblasts from synapse-free regions of denervated muscle, as well as skin, lung, and 3T3 fibroblasts accumulate high levels of tenascin(J1) and fibronectin in culture, showing that perisynaptic fibroblasts are not unique in this regard. However, when they are first placed in culture, fibroblasts from denervated muscle bear more tenascin(J1) than fibroblasts from innervated muscle, indicating that expression of this molecule by fibroblasts is regulated by the muscle's state of innervation; this difference is no longer apparent after a few days in culture. In 3T3 cells, accumulation of tenascin(J1) is high in proliferating cultures, depressed in confluent cultures, and reactivated in cells stimulated to proliferate by replating at low density or by wounding a confluent monolayer. Thus, synthesis of tenascin(J1) is regulated in parallel with mitotic activity. In contrast, levels of fibronectin, which increase less dramatically after denervation in vivo, are similar in fibroblasts from innervated and denervated muscle and in proliferating and quiescent 3T3 cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

Electrical stimulation treatment of dog's denervated orbicularis oculi muscle.

In this investigation, the electrophysiology and pathology of denervated orbicularis oculi muscles have been studied in dogs during chronic electrical stimulation. The orbicularis oculi muscles were unilaterally denervated in 8 dogs, and 4 of these muscles were directly stimulated on a daily basis for 75 days. No difference in minimum stimulus intensities evoking orbicularis oculi muscle twitch contraction appeared between denervated treated and nontreated muscles. A significant reduction of minimum stimulus intensities evoking upper eyelid complete closure (blink), however, was found in the denervated treated muscles between 10 and 30 days (p less than 0.01). At 28 and 75 days, orbicularis oculi muscle biopsies showed no difference in muscle fiber diameter between denervated treated and nontreated muscles. At 75 days, type II muscle fiber distribution, however, was significantly increased in denervated treated muscles compared with denervated nontreated muscles (p less than 0.01). These findings of orbicularis oculi muscle electrophysiology were consistent with a transient reversal of denervation changes by electrical stimulation, partially supported by muscle biopsies.

Animals↗
PubMed2005

Cellular inflammatory response induced by sensory denervation of the conjunctiva in monkeys.

The inflammatory response induced by sensory denervation of the cornea, neuroparalytic (neurotrophic) keratitis, has been widely reported in the literature. Clinical evidence has shown that the conjunctiva also responds to sensory denervation, but little is known of the cytology of the conjunctival tissue response to denervation. The purpose of this study therefore was to investigate the cytological aspects of tissue response induced in the conjunctiva of monkeys by sensory denervation. Intracranial ophthalmic neurotomy was carried out in three monkeys, maxillary neurotomy in four, combined ophthalmic and maxillary neurotomy in two, and infraorbital nerve transaction in one monkey. These various operations were performed for other experimental purposes, but the conjunctival tissues from the animals were suitable and available to study the cytology of the inflammatory response induced in the tissue following the sensory denervation. The cytological changes were studied using light microscopy. Complete or severe ophthalmic nerve transection induced significant inflammatory responses, which were largely confined to the tarsal region of the conjunctiva. The responses included a substantial increase in the infiltration of the epithelium by polymorphonuclear leucocytes and severe disruption of the epithelium. The number of macrophages in the conjunctiva also increased. The response induced by maxillary denervation, however, was not as pronounced as that induced by sensory denervation. The restriction of the conjunctival tissue response to the tarsal region was considered to be due to the friction between the tarsal conjunctiva (and the hard tarsal plate) and the cornea during blinking. This study shows that sensory denervation of the conjunctiva elicits an inflammatory response characterized by substantial infiltration of the epithelium by neutrophil and macrophage and disorganization of the conjunctival tissue.

Animals↗
PubMed1983

Extrasynaptic accumulations of acetylcholinesterase in the rat sternocleidomastoid muscle after neonatal denervation. Light and electron microscopic localization and molecular forms.

Denervated neonatal rat sternocleidomastoid muscle has decreased levels of total AChE when compared to control muscle. Denervated versus control values of total muscle AChE present a three-phase curve in function of time after denervation. There is a rapid initial fall 0-3 days after denervation, an increase during about 2 weeks, then again a decrease in total AChE. Thus, there is a transitory net accumulation of AChE after the initial fall of activity in denervated developing muscle. Extrasynaptic areas of high AChE activity develop between 1 and 2 weeks after denervation and remain visible up to 1 month after denervation before vanishing. An electron microscope study shows that these accumulations are internal to the muscle fiber, close to a limited number of muscle nuclei and associated to the sarcoplasmic reticulum and nuclear envelope, but not to the T-tubule system. As found in adult rat muscle, the initial fall in AChE affects first the 16 S AChE form, and soon after, the 4 S and 10 S AChE forms. A main difference with adult muscle is the sudden increase and predominance over other forms of 10 S AChE 2 weeks after denervation at birth. Later, the decrease in AChE affects 16 S and 4 S AChE before 10 S AChE. The regions rich in extrasynaptic sites of AChE accumulation possess a very high proportion of 10 S AChE. Thus, the mechanisms of biosynthesis, intracellular transport and/or secretion of AChE may be very different in young, developing muscle compared to adult muscle.

Acetylcholinesterase↗
PubMed1986

Effect of denervation on a steady electric current generated at the end-plate region of rat skeletal muscle.

An electric current flows continuously out of the synaptic region of rat lumbrical muscle fibres. It is generated apparently as a result of a non-uniform Cl- conductance (GCl), with GCl being lowest at the end-plate. We investigated the effects of denervation on this current. The current persisted with little change after denervation. This was somewhat unexpected, since GCl falls dramatically after denervation, and in acute experiments on normal muscles, the steady current is greatly reduced by agents which block GCl. The steady current was blocked in denervated muscle, as in normal muscle, by low-Cl- solutions, Na+-free and K+-free solutions, and treatment with furosemide and 9-anthracene-carboxylic acid. The current in denervated muscle appears to be generated by the same general mechanism as in normal muscle. The results suggest that the [Cl-]i is significantly higher in denervated than in normal muscle fibres. Preliminary experiments with Cl- -selective micro-electrodes have confirmed this: [Cl-]i rises from about 12 mM to about 23 mM after denervation. This has the effect of moving the Cl- equilibrium potential (ECl) in a positive direction, so that the driving force for passive Cl- efflux is increased. The increased driving force compensates for the reduced GCl, allowing the steady current to persist in denervated fibres.

Action Potentials↗
PubMed1995

Expression and distribution of sodium channels in short- and long-term denervated rodent skeletal muscles.

1. Loose-patch voltage-clamp recordings were made from rat and mouse skeletal muscle fibres denervated for up to 6 weeks. Innervated muscles possessed a Na+ current density of 107 +/- 3.3 mA cm-2 in endplate membrane, and 6.3 +/- 0.6 mA cm-2 in extrajunctional membrane. This high concentration of Na+ channels at the endplate was gradually reduced following denervation. After 6 weeks of denervation, the endplate Na+ channel concentration was reduced by 40-50%, and the density of Na+ channels in extrajunctional membrane was increased by about 30%. 2. The tetrodotoxin (TTX)-resistant form of the Na+ channel appeared after 3 days of denervation and comprised approximately 43% of the endplate Na+ channels 5-6 days after denervation. Subsequently, TTX-resistant Na+ channels were reduced in density to approximately 25% of the postjunctional Na+ channels and remained at this level up to 6 weeks after denervation. 3. RNase protection analysis showed that mRNA encoding the TTX-resistant Na+ channel was virtually absent in innervated muscle, rose > 50-fold after 3 days of denervation, then decreased by 95% 6 weeks after denervation. The density of TTX-resistant Na+ channels correlated qualitatively with changes in mRNA levels. 4. These results suggest that the density of Na+ channels at neuromuscular junctions is maintained by two mechanisms, one influenced by the nerve terminal and the other independent of innervation.

Animals↗
PubMed2005

M2 and M3 muscarinic receptor activation of urinary bladder contractile signal transduction. II. Denervated rat bladder.

Normal rat bladder contractions are mediated by the M(3) muscarinic receptor subtype. The M(2) receptor subtype mediates contractions of the denervated, hypertrophied bladder. This study determined signal transduction mechanisms mediating contraction of the denervated rat bladder. Denervated bladder muscle strips were exposed to inhibitors of enzymes thought to be involved in signal transduction in vitro followed by a cumulative carbachol concentration-response curve. Outcome measures were the maximal contraction, the potency of carbachol, and the affinity of darifenacin for inhibition of contraction. Inhibition of phosphoinositide-specific phospholipase C (PI-PLC) with 1-O-octadecyl-2-O-methyl-sn-glycero-3-phosphorylcholine (ET-18-OCH(3)) has no effect on denervated bladder contractions, whereas inhibition of phosphatidyl choline-specific phospholipase C (PC-PLC) with O-tricyclo[5.2.1.02,6]dec-9-yl dithiocarbonate potassium salt (D609) attenuates the carbachol maximum and potency. Inhibition of rho kinase with (R)-(+)-trans-4-(1-aminoethyl)-N-(4-pyridyl)cyclohexanecarboxamide dihydrochloride (Y-27632) reduces carbachol maximum, carbachol potency, and increases darifenacin affinity. Inhibition of rho kinase, protein kinase A (PKA), and protein kinase G (PKG) with 1-(5-isoquinolinesulfonyl)-homopiperazine.HCl (HA-1077) reduces the carbachol maximum and potency. Inhibition of PKC with chelerythrine increases darifenacin affinity, whereas inhibition of rho kinase, PKA, PKG, and protein kinase C (PKC) with 1-(5-isoquinolinesulfonyl)-2-methylpiperazine.2HCl (H7) reduces the carbachol potency while increasing darifenacin affinity. Inhibition of rho kinase, PKA, and PKG with N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide.2HCl (H89) increases darifenacin affinity. This study demonstrates that different signal transduction mechanisms mediate the contractile response in the denervated rat bladder than in normal rat bladder. In normal rat bladder, PI-PLC and PC-PLC mediate the contraction, but in denervated bladder only PC-PLC is involved. In the denervated bladder, the rho kinase pathway is more dominant than in normal bladders. PKA seems to mediate a contractile response in normal bladders, whereas it seems to inhibit contraction in denervated bladders.

Animals↗
PubMed2004

In vivo expression patterns of MyoD, p21, and Rb proteins in myonuclei and satellite cells of denervated rat skeletal muscle.

MyoD, a myogenic regulatory factor, is rapidly expressed in adult skeletal muscles in response to denervation. However, the function(s) of MyoD expressed in denervated muscle has not been adequately elucidated. In vitro, it directly transactivates cyclin-dependent kinase inhibitor p21 (p21) and retinoblastoma protein (Rb), a downstream target of p21. These factors then act to regulate cell cycle withdrawal and antiapoptotic cell death. Using immunohistochemical approaches, we characterized cell types expressing MyoD, p21, and Rb and the relationship among these factors in the myonucleus of denervated muscles. In addition, we quantitatively examined the time course changes and expression patterns among distinct myofiber types of MyoD, p21, and Rb during denervation. Denervation induced MyoD expression in myonuclei and satellite cell nuclei, whereas p21 and Rb were found only in myonuclei. Furthermore, coexpression of MyoD, p21, and Rb was induced in the myonucleus, and quantitative analysis of these factors determined that there was no difference among the three myofiber types. These observations suggest that MyoD may function in myonuclei in response to denervation to protect against denervation-induced apoptosis via perhaps the activation of p21 and Rb, and function of MyoD expressed in satellite cell nuclei may be negatively regulated. The present study provides a molecular basis to further understand the function of MyoD expressed in the myonuclei and satellite cell nuclei of denervated skeletal muscle.

Age Factors↗
PubMed1985

Potassium movements in denervated frog sartorius muscle.

The movement of 42K+ across the sarcolemma and the resting membrane potential (VM) of normal and denervated frog sartorius muscle were studied under several experimental conditions in preparations initially equilibrated in 100 mM K+ and 219 mM Cl-. The results can be summarized as follows. In the absence of any driving force on K+, i.e., when the difference between VM and the K+ equilibrium potential (EK) is zero (VM - EK = 0), the K+ conductance (gK) was 368 microseconds . cm-2 in control and 282 microseconds. in denervated muscle. The reduced gK of denervated muscles results from the addition of the opposite changes in the conductances of a Rb+-sensitive inward rectifying pathway (gIR), which decreases, and a Rb+-insensitive linear channel (gL), which increases. Thus in control muscles gK (368 microseconds . cm-2) equals gIR (359 microseconds . cm-2) plus gL (9 microseconds . cm-2), while in denervated muscles gK (282 microseconds . cm-2) equals gIR (198 microsecond . cm-2) plus gL (84 microseconds . cm-2). Denervation significantly reduces the inward rectifying properties of the resting K+ permeability system. In the presence of outward driving forces on K+ (VM - EK greater than 0) of 35-50 mV, the Rb+-sensitive inward rectifier channel appears to close completely in both control and denervated muscles. In the latter, however, the effect was not as well maintained as in the former, suggesting that its closing mechanism might be altered by denervation. No changes were observed during the first 2 wk after denervation.

Animals↗
PubMed1990

Alterations in the functional properties of skinned fibers from denervated rabbit skeletal muscle.

Isometric tension was recorded in vitro from chemically skinned fibers obtained from normal and 14-day-denervated extensor digitorum longus muscles of the rabbit. Denervation potentiated the tensions elicited by pCa 6.0 but did not modify the pCa value (5.6) required for maximum tension. Ca2+ transport across the membranes of the sarcoplasmic reticulum (SR) was markedly affected by denervation. Thus the rate of ATP-dependent net Ca2+ uptake increased significantly, and the spontaneous release ("leakage") of the Ca2+ stored in the SR was significantly reduced in denervated fibers. These effects lead to increased accumulation of Ca2+ in the lumen of the SR. The dose-response curve for the halothane-induced contractures of Ca2(+)-loaded skinned fibers was displaced to the left after denervation. Thus 0.7 mM halothane, a concentration that elicited no tension in 10 control fibers, induced contractures in the 10 denervated fibers tested. The potentiation of the halothane-induced tensions is attributed mainly to the larger stores of Ca2+ in the SR of denervated fibers. The possibility that denervation may also affect the interaction of halothane with the SR membranes is discussed.

Adenosine Triphosphate↗
PubMed1990

Effect of denervation of the myenteric plexus on gastroduodenal motility in turkeys.

The effect of denervation of portions of the myenteric plexus on initiation and coordination of gastric and duodenal contractions was examined in domestic turkeys. Three areas of the muscular stomach (MS), the isthmus between the glandular stomach (GS) and MS, and the pylorus were denervated by application of 1% benzalkonium chloride. Motor activity of the gastroduodenal organs was monitored for 1 h every other day for 13 days using strain gauge transducers implanted at selected sites. Denervation of the isthmus reduced the frequency of MS and duodenal contractions by 50% and abolished GS contractions. Pyloric denervation did not affect the frequency of GS or MS contractions but abolished duodenal contractions. These results suggest that 1) a driving pacemaker for the gastroduodenal cycle is located in the isthmus, and 2) the myenteric plexus is essential for conduction from the pacemaker to the GS and to the duodenum. Denervation of the medial commissure of the myenteric plexus of the MS significantly impaired the function of the ventral half of the MS. It caused atrophy of the underlying medial thick muscle and significantly decreased contraction amplitude. Denervation at this site also caused an enlargement and impaction of the adjacent caudal thin muscle with food and a significant decrease in contraction amplitude. In contrast, denervation of the lateral commissure enlarged the underlying lateral thick muscle and significantly increased its contraction amplitude. Denervation of the cranial thin muscle delayed contractions of that muscle, causing an asynchronization of thin muscle pair.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Pathogenesis of one-kidney, one-clip hypertension in rats after renal denervation.

This study examines the role of the renal nerves in the chronic and early developmental stages of one-kidney, one-clip (1K-1C) Goldblatt hypertension. Groups of uninephrectomized Sprague-Dawley rats underwent renal artery constriction with a clip of an internal diameter of 0.23 mm (groups 1 and 3) or 0.40 mm (groups 2 and 4) to produce severe or moderate hypertension. Two weeks later, groups 1 and 2 were subjected to renal denervation and groups 3 and 4 were denervated 6 and 7 wk after clipping, respectively. In all four groups, hypertension remained unchanged during the subsequent 2 wk after denervation. To study further the effects of renal denervation during the early onset of hypertension, groups 5, 6, and 7 received the smaller (0.23 mm) clip after uninephrectomy. Groups 5 and 6 were renal denervated immediately before clipping; group 7 was not denervated. In groups 6 and 7 the renin-angiotensin system was blocked with a continuous infusion of the converting-enzyme inhibitor captopril for 24 h before and 15 days after clipping. In group 5, renal denervation did not prevent a prompt and severe rise in the systolic blood pressure. In groups 6 and 7, infusion of captopril prevented the hypertension only during the first 4 days after clipping; at no time was there a difference in the systolic blood pressure curves of groups 6 and 7 during or after captopril infusion. These data demonstrate that regardless of the severity and duration of hypertension, renal denervation failed to attenuate either the development or the maintenance of 1K-1C Goldblatt hypertension in the rat. Thus the present results fail to provide support for the concept that the renal nerves modulate the hypertension in this experimental model.

Animals↗