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At least 19 recordsLinked to original sources
PubMed1992

[The effect of prostacyclin (PGI) on denervated tissues--especially, about denervation supersensitivity].

It is well known that contractive agents of smooth muscle have denervation supersensitivity. But, the existence of denervation supersensitivity in relaxed ones does not become so clear. We investigated these supersensitivity, especially prostacyclin (PGI2). We made the denervated artery by lumbar sympathetic ganglionectomy in mongrel dogs. Namely, saphenous and dorsal pedal arteries were denervated by this ganglionectomy. And we studied the changes of these arterial tensions by magnus apparatus. Dose-response (D-R) curves of denervated arteries for KCl and noradrenaline (NE) shifted to left against control arteries. Next, we studied effects of PGI2. At first, we measured ED50 of KCl and NE contraction. And, we produced the half contraction on each artery by using ED50 of KCl and NE. Lastly, PGI2 was added on the half contractive arteries to study relaxed changes. D-R curves of denervated arteries for PGI2 shifted to left, too. These denervated arteries acquired the supersensitivity for PGI2. Clinically, if we use relaxants after organ transplantation, these drugs may be very effective for the perfusion of the grafts.

Animals↗
PubMed1977

Partial denervation affects both denervated and innervated fibers in the mammalian skeletal muscle.

Partial denervation of the rat extensor digitorum longus muscle was performed by sectioning only one of the sciatic nerve roots. Measurements of spike resistance to tetrodotoxin in individual muscle fibers revealed denervation changes not only in the denervated fibers but also in the adjacent innervated ones. The results support the concept that products of nerve degeneration play a role in the origin of muscle changes induced by denervation.

Action Potentials↗
PubMed1992

Unilateral vagal denervation suppresses omeprazole-induced trophic effects on the denervated side of the rat stomach.

In several experimental animals treatment with large doses of the proton pump inhibitor omeprazole leads to hypergastrinemia and with time to trophic effects in the acid-producing part of the stomach, most notably an increased density of the histamine-producing enterochromaffin-like (ECL) cells. The trophic effects are thought to reflect the increase in circulating gastrin. In the present study unilateral vagal denervation in the rat partly suppressed the tropic effects seen in the denervated side of the stomach but not those in the intact side after treatment with omeprazole for 10 weeks. Unilateral vagal denervation significantly reduced the proliferative stimulus of omeprazole on the ECL cells in the denervated part of the stomach. Thus, an intact vagal innervation appears to be essential for the capacity of the oxyntic mucosa, including the ECL cells, to respond to elevations in serum gastrin. We suggest that gastrin and the vagus interact to maintain trophic control of the oxyntic glands.

Animals↗
PubMed1978

Effects of denervation on the rate of entry of inorganic phosphate into rat slow and fast muscles: selective inhibition of denervation changes by actinomycin D.

Actinomycin D abolishes the post denervation increase in inorganic phosphate flow observed in the fast gastrocnemius muscle. In the slow soleus muscle, the initial decrease in phosphate flow is unaffected but the secondary rise is suppressed in the same manner as in the fast muscle. These observations put the post denervation increase in inorganic phosphate flow on a par with the development of extrajunctional cholinergic receptors in being the result of the synthesis of new proteins. It has the added advantage of being suitable to quantitative assessment at the whole muscle level.

Animals↗
PubMed1975

Involvement of adenylate cyclase in mechanisms of denervation supersensitivity following surgical denervation of the dog heart.

Following surgical disruption (4-16 weeks) of the nerves supplying the dog heart, catecholamine (norepinephrine and epinephrine) levels in the atria and ventricles were markedly reduced. Using the 10,000 g particulate fraction as an enzyme source, the activation of adenylate cyclase by norepinephrine was considerably greater in the denervated myocardial preparations (atria and ventricles) than in control hearts. Moreover, in the denervated ventricular preparation fluoride (5 and 10mM) elicited a significantly greater stimulation of the enzyme than that observed in the controls.

Adenylyl Cyclases↗
PubMed1992

Calcium current activation and charge movement in denervated mammalian skeletal muscle fibres.

1. Calcium current (ICa) activation was studied in denervated 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. Controls were normal fibres from non-operated rats. Electrical recordings were carried out using the double Vaseline-gap technique. 2. Current-voltage (I-V) curves showed that the ICa amplitude increased during the first 4-6 days after denervation and subsequently decreased during the second week. Between days 4 and 6 after denervation, the peak ICa amplitude (at 0 mV) was -5.9 +/- 0.5 microA/microF (mean +/- S.E.M.) as compared with -4.8 +/- 0.3 microA/microF in normal fibres. Between days 14 and 15 after denervation, the ICa amplitude was -2.9 +/- 0.4 microA/microF. 3. The time constant of ICa activation (tau a) was significantly increased by denervation. At 0 mV, tau a in normal fibres was 44.8 +/- 1.4 ms. Between 4 and 6 days after denervation tau a was 58.1 +/- 4.8 ms, and between 14 and 15 days after denervation, 55.8 +/- 3.8 ms. 4. The time constant of deactivation (tau d) decreased after denervation. At -10 mV, the tau d in normal fibres was 103.4 +/- 14 ms. The value decreased to 74.5 +/- 8.6 and 74.0 +/- 17 ms between days 4 and 6 and days 14 and 15 of denervation respectively. 5. Charge movement (Qon) was reduced progressively without major changes in the steepness (k) and position on the voltage axis of the Qon-Vm relationship. The fitted parameters under control were Qmax = 15.4 nC/microF, mid-point potential Vq1/2 = -25.2 mV and k = 11.9 mV. Between days 14 and 15 of denervation, the values for Qmax, Vq1/2 and k were 6.7 nC/microF, -36.8 mV and 11.3 mV respectively. 6. Calcium permeability (PCa) in normal and denervated fibres at stages during denervation was calculated according to the Hodgkin-Huxley model. At 0 mV PCa was 1.24 x 10(-5) cm/s in normal fibres, and 7.43 x 10(-6) cm/s after 2 weeks of denervation. 7. The m infinity-Vm relationship was shifted to more positive potentials after denervation without significant changes in the steepness factor k. The V1/2 value in normal fibres was -4.4 mV, and 5.8 mV after two weeks of denervation. 8. The ICa sensitivity to nifedipine was not modified in the different groups of denervated fibres studied. With 10 microM-nifedipine, the 1-(ICa in nifedipine/ICa control) relationships were 0.74 +/- 0.03 in normal fibres and 0.76 +/- 0.12, 14 days after denervation.

Action Potentials↗
PubMed2022

Lipid hydroperoxides and oxylipins are mediators of denervation induced muscle atrophy.

Loss of innervation is a key driver of age associated muscle atrophy and weakness (sarcopenia). Our laboratory has previously shown that denervation induced atrophy is associated with the generation of mitochondrial hydroperoxides and lipid mediators produced downstream of cPLA2 and 12/15 lipoxygenase (12/15-LOX). To define the pathological impact of lipid hydroperoxides generated in denervation-induced atrophy in vivo, we treated mice with liproxstatin-1, a lipid hydroperoxide scavenger. We treated adult male mice with 5 mg/kg liproxstain-1 or vehicle one day prior to sciatic nerve transection and daily for 7 days post-denervation before tissue analysis. Liproxstatin-1 treatment protected gastrocnemius mass and fiber cross sectional area (∼40% less atrophy post-denervation in treated versus untreated mice). Mitochondrial hydroperoxide generation was reduced 80% in vitro and by over 65% in vivo by liproxstatin-1 treatment in denervated permeabilized muscle fibers and decreased the content of 4-HNE by ∼25% post-denervation. Lipidomic analysis revealed detectable levels of 25 oxylipins in denervated gastrocnemius muscle and significantly increased levels for eight oxylipins that are generated by metabolism of fatty acids through 12/15-LOX. Liproxstatin-1 treatment reduced the level of three of the eight denervation-induced oxylipins, specifically 15-HEPE, 13-HOTrE and 17-HDOHE. Denervation elevated protein degradation rates in muscle and treatment with liproxstatin-1 reduced rates of protein breakdown in denervated muscle. In contrast, protein synthesis rates were unchanged by denervation. Targeted proteomics revealed a number of proteins with altered expression after denervation but no effect of liproxstain-1. Transcriptomic analysis revealed 203 differentially expressed genes in denervated muscle from vehicle or liproxstatin-1 treated mice, including ER stress, nitric oxide signaling, Gαi signaling, glucocorticoid receptor signaling, and other pathways. Overall, these data suggest lipid hydroperoxides and oxylipins are key drivers of increased protein breakdown and muscle loss associated with denervation induced atrophy and a potential target for sarcopenia intervention.

Male↗
PubMed1976

The adrenergic innervation and adrenergic receptor activity of the feline urinary bladder and urethra in the normal state and after hypogastric and/or parasympathetic denervation.

After long-term parasymphatetic denervation, detrusor muscle hypertrophy was found regardless of whether the hypogastric nerves had been sectioned simultaneously or not. After hypogastric denervation only, there was no difference in gross appearance from normal bladders. Adrenergic innervation was studied by means of a histochemical fluorescence technique. After hypogastric denervation, there was usually a slight increase in the detrusor innervation, and a clear decrease in the trigone and urethral adrenergic innervation. After parasympathetic denervation, the detrusor showed an increase in adrenergic innervation, while the innervation of the trigone and the urethra was unchanged. After simultaneous parasympathetic and hypogastric denervation, the adrenergic innervation of the detrusor was similar to that of the bladders subjected to parasympathetic denervation only. The adrenergic innervation of the trigone and urethra was similar to that found after hypogastric denervation only. Adrenergic receptor functions were studied by a method in which changes in the isometric tension of muscle strips were recorded following different pharmacological treatments. In the normal state, noradrenalin and phenylephrine caused contraction and isoprenaline relaxation of the trigone-urethra. In the detrusor, noradrenalin caused relaxation of strips contracted by carbacholine. Relaxed detrusor muscle strips were usually not contracted by noradenalin. In 2 out of 8 normal cats, however, a contraction was observed after very large doses of noradrenalin. After hypogastric denervation, the adrenoreceptor functions were consistent with those of the normal state. After parasympathetic denervation, the trigone-urethral receptor functions were unchanged compared with the normal receptor functions. In the detrusor, isoprenaline caused relaxation and noradrenalin and phenylephrine contraction. After simultaneous parasympathetic and hypogastric denervation, the results were consistent with those obtained after parasympathetic denervation only. Thus, the present study showed an increased adrenergic detrusor innervation and alpha-receptor activity after parasympathetic denervation regardless of whether the hypogastric nerves had been sectioned simultaneously or not. Although alpha-receptors might exist in the normal detrusor, beta-receptors dominate strongly. After parasympathetic denervation, there seems to be a change in the relation between alpha- and beta-receptors in favour of alpha-receptors.

Animals↗
PubMed1975

Effects of acute unilateral renal denervation in the rat.

Studies were undertaken to characterize the renal responses to acute unilateral renal denervation and the mechanisms involved in these responses. Denervation was produced in anesthetized nondiuretic rats by application of phenol to the left renal artery. Studies were also performed in sham-denervated nondiuretic rats. Whole kidney and individual nephron studies were performed before and after denervation or sham denervation. Denervation increased urine volume from the left kidney to about twice its control value (P less than 0.001) and increased urinary sodium excretion from 332 neq min minus -1 to 1,887 neq min minus -1 (P less than 0.001). Glomerular filtration rate (GFR) and renal plasma flow (RPF) remained unchanged in both kidneys after the procedure. The innervated right kidney showed no changes in urine volume or in sodium excretion. After denervation, late proximal ratio of tubular fluid inulin concentration to that of plasma [(F/P)In] decreased from 2.23 to 1.50 (P less than 0.001) while single nephron GFR remained unchanged. Absolute reabsorption decreased from 16.5 to 9.9 n. min minus -1 (P less than 0.001). (F/P)In ratios were also decreased in early distal (from 6.21 to 3.18, P less 0.001) and late distal convolutions (from 16.41 to 8.33, P less than 0.001) during the experimental period. (F/P)Na ratios remained unchanged in the early distal convolutions, but increased from 0.18 to 0.38 (P less than 0.01) in late distal convolutions after denervation. Absolute Na reabsorption after denervation increased in the loop of Henle, distal convolution, and collecting ducts. Any changes in intrarenal hydrostatic pressures after denervation were always small. There were no changes in GFR, RPF, urine volume, urinary sodium excretion, or late proximal (F/P)In after sham denervation. We conclude that the diuresis and natriuresis seen after acute renal denervation were caused by a marked depression of sodium and water reabsorption in the proximal tubule with partial compensation in more distal nephron segments. These responses appeared to be unrelated to systemic or intrarenal hemodynamic changes. The results demonstrate an effect of the renal nerves on proximal tubular function.

Aminohippuric Acids↗
PubMed1991

Effects of surgical sympathetic denervation on myo-inositol trisphosphate production and contraction in the dilator and sphincter smooth muscles of the rabbit iris: evidence for interaction between the cyclic AMP and calcium signaling systems.

The effects of norepinephrine (NE), carbachol (CCh), NaF, 3-isobutyl-1-methylxanthine (IBMX), and high K+ concentration (80 mM) depolarization on inositol trisphosphate (IP3) accumulation, cyclic AMP (cAMP) formation, and contraction were investigated in the dilator and sphincter smooth muscles of the sympathetically denervated as well as the normal rabbit eye. (a) In the denervated dilator muscle, NE-stimulated IP3 production and contraction are enhanced. (b) In the sphincter muscle of rabbits that have undergone sympathetic denervation. CCh-stimulated IP3 production and contraction are attenuated. (c) The increase in tension by a maximal effective dose of NaF (209 mM) in the dilator was 12.5 and 18 mg of tension/mg wet weight in normal and denervated tissue, respectively, and in the sphincter was 33.8 and 15.2 mg of tension/mg wet weight in normal and denervated tissue, respectively. NaF had no effect on cAMP formation. (d) Addition of NE had no effect on cAMP formation in both the normal and denervated dilator, whereas basal and IBMX-induced cAMP formation increased. in the denervated sphincter over that of the normal tissue by 15 and 60%, respectively. (e) Isoproterenol (5 microM) increased cAMP formation in the normal and denervated sphincter by 47 and 91%, respectively. (f) Whereas CCh inhibits cAMP formation in the normal sphincter, it lost its inhibitory effect in the sphincter with denervation. (g) IBMX (0.1 mM) attenuated the CCh-stimulated IP3 production and contraction of the sphincter by approximately 30% of their respective controls. (h) High K+ concentration depolarization attenuated contraction in both dilator and sphincter muscles with denervation. These observations suggest that an increase in the level of cAMP in the iris sphincter due to sympathetic denervation could lead to inhibition of phospholipase C (or other target sites, such as phosphorylation of the muscarinic receptor, Gp protein itself, myosin light chain kinase, or the IP3 receptor), IP3 production, and contraction. In conclusion, we suggest that the supersensitivity and subsensitivity observed after surgical sympathetic denervation of the iris dilator and sphincter muscles, respectively, are caused by alterations in the efficiency of coupling, probably through the Gp proteins, between their respective receptors and the breakdown of polyphosphoinositides by phospholipase C. In addition, we propose that the sympathetic nervous system can regulate, through alterations in cAMP levels, the muscarinic stimulation of IP3 accumulation and contraction in the iris sphincter. These findings add further support to the hypothesis that there are reciprocal interactions between the cAMP and IP3-Ca2+ signaling systems and the contractile response in the iris smooth muscle.

1-Methyl-3-isobutylxanthine↗
PubMed1992

The effects of liver denervation on the regulation of hepatic biliary secretion.

Effects of liver denervation on bile formation were studied in eight dogs prepared with chronic biliary fistulas. The animals were studied in the basal state, after feeding, and during infusion of glucagon 50 ng/kg/min, secretin 2 U/kg/hr, or somatostatin 200 ng/kg/min. After this first set of experiments the animals underwent a total hepatic denervation that consisted of section of the hepatic ligaments and a careful dissection of the portal vein, hepatic artery, and common duct with stripping of all the surrounding connective tissue and topical application of phenol. The above experiments were then repeated. Denervation did not modify bile flow, or bile salts, cholesterol, or phospholipid concentration or output. Biliary response to glucagon and secretin was similar before and after denervation. Somatostatin had an anticholerectic effect in both intact and denervated animals, but significantly reduced bile salt output only in the intact dogs. Feeding had a choleretic effect pre- and postdenervation, and the infusion of somatostatin following feeding decreased bile flow to the same degree before and after denervation. In the intact animals the output of all three biliary lipids was reduced by somatostatin after feeding but they were unaffected by somatostatin after denervation. Moreover, cholesterol and phospholipid outputs were stable after feeding in intact animals, but significantly decreased after denervation. 14C-erythritol clearance studies indicated no change in the canalicular component of bile flow with denervation, except again during somatostatin suppression of feeding. These data indicate that basal bile flow is normal after denervation but that innervation may play an important role in the modulation of responses to somatostatin and more complex stimuli such as feeding.

Animals↗
PubMed1975

Influence of activity on the passive electrical properties of denervated soleus muscle fibres in the rat.

The technique of direct electrical stimulation of denervated muscle was used to study the role of muscle activity per se in controlling the passive electrical properties of muscle fibres. 2. Specific membrane resistance and capacitance of the denervated and the denervated-stimulated muscle fibres were measured by a sinewave technique at frequencies between 5 and 240 Hz. The parameter values were constant at low frequencies up to a variable transition frequency and declined rapidly at higher frequencies. 3. Following denervation the low-frequency value of specific membrane resistance increased (2291 omega cm2 for 19-day denervated fibres vs. 766 omega cm2 for innervated fibres), the specific membrane capacitance declined (2-7 muF/cm2 vs. 3-6 muF/cm2) and the transition frequency shifted towards lower frequencies. The specific internal resistance was higher in denervated fibres (301 omega cm for 19-day denervated fibres vs. 240 omega cm in innervated fibres) apart from a transient decline after 5 days of denervation (164 omega cm). 4. Direct electrical stimulation for 2 weeks beginning on the 5th day after denervation restored all parameters listed above to their original values before denervation. 5. Stimulation arrested in most cases further atrophy from the time of stimulation but did not restore normal fibre size.

Animals↗
PubMed1977

Cation movements in normal and short-term denervated rat fast twitch muscle.

1. The earliest known change in rat fast muscle following denervation is a fall in resting membrane potential unaccompanied by change in membrane resistance. The present study tested the hypothesis that increased Na permeability (P(Na)) accounted for this early depolarization.2. In all experiments, rat extensor digitorum longus muscles were studied in vitro at 25 degrees C. Li uptake in vitro, used as a measure of P(Na), was greater in 1- and 2-day denervated muscles (and in 2-day denervated diaphragm) than in paired controls.3. The extra Li taken up by denervated muscle was not sequestered in an extracellular or freely exchangeable compartment, nor was it irreversibly bound.4. Measurements of resting membrane potential and of internal Na, K, and Li in Krebs solution before and 2 hr after replacement of NaCl by LiCl, were used to compute the ratios P(Na)/P(K) and P(Li)/P(K) for normal or denervated muscles. P(Na) and P(Li) were similar relative to P(K) within each class of muscle.5. Both P(Na)/P(K) and P(Li)/P(K) ratios were elevated more than twofold in denervated muscle, as were most estimates of relative P(Li) approximated by the flux equation.6. These data, and measurement of resting membrane potential of normal muscle in 1 mM external K-Krebs solution, support the view that an electrogenic Na-K pump does not substantially contribute to this potential of normal or denervated muscle, and that the early depolarization after denervation results from increased P(Na).7. The Na-K pump of denervated muscle was as sensitive to ouabain as normal muscle. An effect of ouabain on P(Na) may explain previously noted differential effects of ouabain on normal and denervated muscle.

Animals↗
PubMed1979

Effect of acute and chronic renal denervation on renal function after release of unilateral ureteral obstruction in the rat.

The role of the renal nerves in determining renal function after relief of 24-h unilateral ureteral obstruction (UUO) was studied using clearance techniques in anaesthetized rats. Acute renal denervation during the first 1--2 h after relief of UUO resulted in a significant increase in glomerular filtration rate (GFR), renal plasma flow (RPF), urine flow, and sodium and potassium excretion, changes which were not seen in the sham-denervated postobstructive kidney. Acute denervation of sham-operated normal kidneys caused a similar natriuresis and diuresis but with no change in GFR or RPF. Chronic renal denervation 4--5 days before UUO denervated postobstructive controls, while chronic denervation alone was associated with a significantly higher urine flow and sodium excretion rate from the denervated kidney. The effectiveness of renal denervation was confirmed by demonstrating marked depletion of tissue catecholamines in the denervated kidney. It was concluded that renal nerve activity plays a significant but not a major role in the functional changes present after relief of UUO. Chronic renal denervation did not protect against the functional effects of unilateral ureteral obstruction.

Animals↗
PubMed1992

Recovery of arterial pressure control after partial baroreceptor denervation in awake rabbits.

We examined recovery of control of heart rate (HR) and total peripheral resistance (TPR) by arterial baroreceptors after bilateral carotid sinus and aortic denervation or unilateral carotid sinus and aortic denervation in conscious rabbits. In one group of animals, HR responses to changes in mean arterial pressure (MAP) after injection of nitroglycerin or phenylephrine were measured in control studies and at 2, 5, 10, and 15 days after partial baroreceptor denervation. All denervation procedures increased MAP and HR at 2 and 5 days after denervation. Reflex sensitivity decreased to 57-67% of control on day 2 after denervation. HR responses recovered by day 10 after bilateral aortic or carotid sinus denervation; however, recovery following unilateral denervation was less complete. In a second group of animals, studied after implantation of aortic flowmeters, TPR changes following reduction in cardiac output by inferior vena caval occlusion were 49% of control responses on day 2 after denervation and returned close to control level on day 5. Controls of HR and TPR recovered substantially and were not significantly different from control 10 days after partial denervation. Recovery apparently occurred through the remaining arterial baroreceptors, possibly due to central reorganization of reflex pathways.

Animals↗
PubMed1992

Re-innervation of submucosal arterioles by myenteric neurones following extrinsic denervation.

We used a combination of selective lesions, immunohistochemistry and video monitoring of arteriolar diameter to determine the source of the changes in vasodilator innervation to guinea pig ileal submucosal arterioles which occur following removal of their extrinsic sympathetic and sensory nerve fibre input. A non-cholinergic neurogenic vasodilation appeared in arterioles in which extrinsic denervation was performed 50-90 days previously. The non-cholinergic innervation did not result from regrowth of extrinsic fibres because the neurogenic response was not altered by combining long-term denervation with capsaicin treatment or re-denervation 7 days prior to examination. However, non-cholinergic neurogenic vasodilations were not observed in arterioles which had been subjected to long-term denervation combined with a myectomy 7 days prior to examination. Immunohistochemical co-localization of SP and CGRP in these vessels confirmed previous findings that a prominent SP perivascular nerve plexus appeared after long-term denervation. Perivascular SP-containing fibres that appeared after long-term denervation were unaffected by capsaicin or re-denervation but were absent from preparations in which long-term denervation and myectomy were performed. These results demonstrate that myenteric neurones are the source of the non-cholinergic innervation which appears after extrinsic denervation and support our previous conclusion that SP is the neurotransmitter responsible for this non-cholinergic vasodilation in submucosal arterioles of the small intestine.

Animals↗