bluuebunny/crossref_metadata_2025_split huggingface dataset:
Necessity of acetylcholine for retinal directionally selective responses to drifting gratings in rabbit
Authors: Grzywacz Norberto M. , Amthor Franklin R. , Merwine David K. 
Published: September 2004

A model for retinal directional selectivity postulates that GABAergic inhibition of responses to motions in the null (anti‐preferred) direction underlies this selectivity. An alternative model postulates that besides this inhibition, there exists an asymmetric, nicotinic acetylcholine (ACh) input from starburst amacrine cells. It is possible for the latter but not the former model that stimuli could exist such that nicotinic blockade eliminates directional selectivity. Such stimuli would drive the cholinergic but not the GABAergic system well.So far, attempts to eliminate directional selectivity with nicotinic blockade have failed, but they always used isolated, moving bars as the stimulus. We confirmed this failure for On‐Off directionally selective (DS) ganglion cells in our preparation of the rabbit's retina.However, while recording from these cells, we discovered that nicotinic blockade eliminated directional selectivity to drifting, low spatial frequency sine‐ and square‐wave gratings.This effect was not just due to the smallness of the responses under nicotinic blockade. NMDA blockade caused even smaller responses, but no loss of directional selectivity.This result is consistent with a two‐asymmetric‐pathways model of directional selectivity, but inconsistent with an asymmetric‐GABA‐only model.We conclude that asymmetric nicotinic inputs extend the range of stimuli that can elicit directional selectivity to include moving textures, that is, those with multiple peaks in their spatial luminance profile.
Focally recorded single sympathetic postganglionic neuronal activity supplying rat lateral tail vein
Authors: Johnson Christopher D. , Gilbey Michael P. 
Published: September 2004

In anaesthetized rats, using a focal recording technique, activity was recorded from single sympathetic postganglionic neurones innervating the lateral tail veins. On‐going activity was examined in order to determine whether it had similar or different characteristics to those recorded from the caudal ventral artery in a previous study.
Animals were artificially ventilated, vagotomized, paralysed and given a pneumothorax.
The discharges of fourteen out of seventeen sympathetic postganglionic neurones were rhythmic. Such units had a mean firing frequency of 1.62 ± 0.70 Hz. The mean frequency of the dominant sympathetic rhythm under control conditions was 0.82 ± 0.05 Hz.
The frequency of the dominant sympathetic rhythm was different from that of the phrenic rhythm in nine out of fourteen cases.
The mean frequency of the dominant sympathetic rhythm was: (i) not influenced significantly by hypocapnic apnoea, (ii) decreased by hyperthermia, which increased the frequency of the phrenic rhythm, (iii) in all cases different from that of the artificial ventilation cycle.
The above characteristics are similar to those recorded from the sympathetic supply to the caudal ventral artery of the same vascular bed under comparable conditions.
Mechanisms of Ca2+ sensitization of force production by noradrenaline in rat mesenteric small arteries
Authors: Buus Carsten L. , Aalkjær Christian , Nilsson Holger , Juul Birte , Møller Jesper V. , Mulvany Michael J. 
Published: September 2004

Mechanisms of Ca2+ sensitization of force production by noradrenaline were investigated by measuring contractile responses, intracellular Ca2+ concentration ([Ca2+]i) and phosphorylation of the myosin light chain (MLC) in intact and α‐toxin‐permeabilized rat mesenteric small arteries.
The effects of noradrenaline were investigated at constant membrane potential by comparing fully depolarized intact arteries in the absence and presence of noradrenaline. Contractile responses to K‐PSS (125 mM K+) and NA‐K‐PSS (K‐PSS + 10 μM noradrenaline) were titrated to 30 and 75 %, respectively, of control force, by adjusting extracellular Ca2+ ([Ca2+]o). At both force levels, [Ca2+]i was substantially lower with NA‐K‐PSS than with K‐PSS. With K‐PSS, the proportion of MLC phosphorylated (≈30 %) was similar at 30 and 75 % of control force; with NA‐K‐PSS, MLC phosphorylation was greater at the higher force level (40 vs. 34 %).
In α‐toxin‐permeabilized arteries, the force response to 1 μM Ca2+ was increased by 10 μM noradrenaline, and MLC phosphorylation was increased from 35 to 45 %. The protein kinase C (PKC) inhibitor calphostin C (100 nM) abolished the noradrenaline‐induced increase in MLC phosphorylation and contractile response, without affecting the contraction in response to Ca2+. Treatment with ATPγS in the presence of the MLC kinase inhibitor ML‐9 increased the sensitivity to Ca2+ and abolished the response to noradrenaline.
The present results show that in rat mesenteric small arteries noradrenaline‐induced Ca2+ sensitization is associated with an increased proportion of phosphorylated MLC. The results are consistent with a decreased MLC phosphatase activity mediated through PKC. Furthermore, while MLC phosphorylation is a requirement for force production, the results show that other factors are also involved in force regulation.
Buffering of blood pressure variability by the renin‐angiotensin system in the conscious dog
Authors: Just Armin , Kirchheim Hartmut R. , Ehmke Heimo 
Published: September 2004

The renin‐angiotensin system (RAS) participates in the compensation of major blood pressure disturbances such as haemorrhage and is involved in the tonic long‐term (> 1 day) maintenance of mean arterial blood pressure (MABP). Since its contribution to the short‐term (< 1 h) buffering of normal blood pressure variability is not known, this was investigated in resting conscious dogs.
The regulatory efficiency and the response time of the RAS were studied by an acute step reduction of renal artery pressure to 70 mmHg for 1 h using a suprarenal aortic cuff. After a delay of at least 100 s, MABP rose exponentially by 22 ± 5 mmHg in normal dogs (n= 4), by 6 ± 3 mmHg after angiotensin converting enzyme (ACE) inhibition (n= 4), and by 25 ± 5 mmHg after ganglionic blockade (n= 4). MABP returned to control after release of the cuff with similar time courses. The time constants of the MABP responses were in the range of 20 min. Thus, possible feedback oscillations of the RAS would be expected around 0.0025 Hz (1/(4 × 100 s)); a buffering effect would be possible below this frequency.
Blood pressure variability was investigated by spectral analysis of MABP from 3.75 h recordings in the frequency ranges of 0.002–0.003 Hz (feedback oscillations) and below 0.002 Hz (buffering effect).
ACE inhibition (n= 7) decreased MABP by 11 ± 2 mmHg (P < 0.05), but in both frequency ranges integrated spectral density was not affected. ACE inhibition also failed to significantly change spectral density in either of the two frequency ranges under the following conditions: (1) during ganglionic blockade (n= 7), (2) during a low‐sodium diet (except for a very slight elevation below 0.002 Hz) (n= 7), and (3) when the fall of MABP induced by ACE inhibition was compensated by an angiotensin II infusion (n= 7).
It is concluded that in spite of its high regulatory efficiency with an adequate response time the RAS does not directly contribute to the short‐term buffering of blood pressure variability, nor does it give rise to feedback oscillations under normal resting conditions. Even if the RAS is stimulated by sodium restriction its contribution to short‐term blood pressure buffering is only marginal.
Shortening‐induced force depression in human adductor pollicis muscle
Authors: De Ruiter C. J. , De Haan A. , Jones D. A. , Sargeant A. J. 
Published: September 2004

The effects of single isovelocity shortening contractions on force production of the electrically stimulated human adductor pollicis muscle were investigated in seven healthy male subjects.
Redeveloped isometric force immediately following isovelocity shortening was always depressed compared with the isometric force recorded at the same muscle length but without preceding shortening. The maximal isometric force deficit (FD) was (mean ± s.e.m.) 37 ± 2 % after 38 deg of shortening at 6.1 deg s−1.
The FD was positively correlated with angular displacement (r2 > 0.98) and decreased with increasing velocity of the shortening step. Stimulation at 20 Hz instead of 50 Hz reduced absolute force levels during the contractions to about 73 % and the FD was decreased to a similar extent. Eighty‐nine per cent of the velocity‐related variation in the FD could be explained by the absolute force levels during shortening.
FD was largely abolished by allowing the muscle to relax briefly (approximately 200 ms), a time probably too short for significant metabolic recovery.
At all but the highest velocities there was a linear decline in force during the latter part of the isovelocity shortening phase, suggesting that the mechanisms underlying FD were active during shortening.
Our results show that shortening‐induced force deficit is a significant feature of human muscle working in situ and is proportional to the work done by the muscle‐tendon complex. This finding has important implications for experimental studies of force‐velocity relationships in the intact human.
Role of insulin‐like growth factor binding proteins in human post‐nephrectomy proximal tubule cells
Authors: Johnson David W. , Saunders Heather J. , Field Michael J. , Pollock Carol A. 
Published: September 2004

In order to determine the role of the insulin‐like growth factor‐I (IGF‐I)/IGF binding protein (IGFBP) axis in the augmentation of tubule growth and function following reductions in nephron mass, primary cultures of human proximal tubule cells (PTCs) were generated from the histologically normal sections of ten surgically removed kidneys.
PTC hypertrophy (cellular protein content), DNA synthesis (thymidine incorporation) and apical sodium‐hydrogen exchange (NHE) activity (ethylisopropylamiloride‐sensitive apical 22Na+ uptake) were measured following 24 h incubation in media supplemented with 10 % pre‐ or post‐nephrectomy sera obtained from these patients. The results were compared with the effects of pre‐ and post‐operative control sera collected from seven patients undergoing retroperitoneal operations not involving removal of renal tissue.
Day 1 post‐nephrectomy sera promoted a significant 73 % increase in apical NHE activity, which was accompanied by a significant increase in PTC binding of 125I‐IGF‐I (post‐ vs. pre‐nephrectomy, 163 ± 6 vs. 142 ± 4 fmol (mg protein)−1; P < 0.05). Subsequent post‐nephrectomy sera significantly stimulated PTC protein content and thymidine incorporation, peaking at day 7 (127.7 ± 14.0 and 118.4 ± 9.0 % of pre‐nephrectomy values, respectively; P < 0.05). The growth effects were cell specific, as they were not observed with renal cortical fibroblasts. No change was detected in any of these measured variables following exposure to control sera.
Serum IGF‐I and IGFBP‐1 levels did not significantly change over time or between groups. IGFBP‐3 levels progressively decreased in both control and nephrectomized sera from pre‐operative values of 3580 ± 305 and 3360 ± 217 ng ml−1, respectively, to 2670 ± 341 and 2600 ± 347 ng ml−1 at 1 week post‐operation. Serum IGFBP‐2 levels increased to a comparable extent in both controls (day 0 vs. day 7, 2940 ± 1024 vs. 7010 ± 2520 ng ml−1; P < 0.01) and nephrectomized patients (day 0 vs. day 7, 3070 ± 656 vs. 9130 ± 2010 ng ml−1; P < 0.01).
The results indicate that nephrectomy engenders the elaboration of one or more humoral factor(s), which promotes increased binding of IGF‐I to PTCs and which may in turn specifically stimulate PTC Na+ transport and growth.
Modification of Cl− transport in skeletal muscle of Rana temporaria with the arginine‐binding reagent phenylglyoxal
Authors: Skydsgaard Jørgen M. 
Published: September 2004

The effect of membrane modification by the arginine‐binding reagent phenylglyoxal (PG) on Cl− permeability was studied in thin bundles of twitch fibres from frog muscle. The bundles were modified by a method that yields stable PG binding to outer arginyl residues in erythrocyte membranes.
PG almost eliminated the pH‐dependent fraction of 36Cl− efflux under conditions of Cl− equilibrium in depolarized bundles: the fluxes at pH 7.2 and 8.5 were strongly inhibited approaching an apparent baseline value close to the normal flux at pH 6 which per se was not inhibited.
The uninhibited flux at pH 6 in modified bundles maintained the normally high sensitivity to DNDS), and the reduction of fluxes at pH > 7 coincided with increased DNDS sensitivity, suggesting a selective blocking of the pH‐dependent flux fraction that has a low DNDS sensitivity.
In normal Ringer solution the modified fibres showed normal resting membrane potentials (Vm) with normal sensitivity to [K+]o but sensitivity to changes of [Cl−]o was almost eliminated, suggesting a normal resting Na+ : K+ conductance ratio (gNa/gK) and that the main influence of modification on the resting membrane conductance (gm) was a loss of Cl− conductance (gCl).
The modified fibres were not excitable, possibly due to arginine modification in the voltage sensor (S4) of the Na+ channels.
These results suggest that positively charged arginines are important for the activity of the pH‐dependent Vm‐stabilizing Cl− channels and that PG may isolate a pH‐independent ‘basal’ flux fraction which normally dominates the Cl− flux at low pH.
Compensatory and excess retrieval: two types of endocytosis following single step depolarizations in bovine adrenal chromaffin cells
Authors: Engisch Kathrin L. , Nowycky Martha C. 
Published: September 2004

Endocytosis following exocytosis evoked by single step depolarizations was examined in bovine adrenal chromaffin cells using high resolution capacitance measurements in perforated‐patch voltage clamp recordings.
Endocytosis was detected as a smooth exponential decline in membrane capacitance to either the pre‐stimulus level (‘compensatory retrieval’) or far below the pre‐stimulus level (‘excess retrieval’). During excess retrieval, > 10 % of the cell surface could be internalized in under 5 s.
Compensatory retrieval was equal in magnitude to stimulus‐evoked exocytosis for membrane additions > 100 fF (about fifty large dense‐cored vesicles). In contrast, excess retrieval surpassed both the stimulus‐evoked exocytosis, and the initial capacitance level recorded at the onset of phase‐tracking measurements. Cell capacitance was not maintained at the level achieved by excess retrieval but slowly returned to pre‐stimulus levels, even in the absence of stimulation.
A large percentage of capacitance increases < 100 fF, usually evoked by 40 ms depolarizations, were not accompanied by membrane retrieval.
Compensatory retrieval could occur with any amount of Ca2+ entry, but excess retrieval was never triggered below a threshold Ca2+ current integral of 70 pC.
The kinetics of compensatory and excess retrieval differed by an order of magnitude. Compensatory retrieval was usually fitted with a single exponential function that had a median time constant of 5.7 s. Excess retrieval usually occurred with double exponential kinetics that had an extremely fast first time constant (median, 670 ms) and a second time constant indistinguishable from that of compensatory retrieval.
The speed of compensatory retrieval was Ca2+ dependent: the largest mono‐exponential time constants occurred for the smallest amounts of Ca2+ entry and decreased with increasing Ca2+ entry. The Ca2+ dependence of mono‐exponential time constants was disrupted by cyclosporin A (CsA), an inhibitor of the Ca2+‐ and calmodulin‐dependent phosphatase calcineurin.
CsA also reduced the proportion of responses with excess retrieval, but this action was caused by a shift in Ca2+ entry values below the threshold for activation. The lower total Ca2+ entry in the presence of CsA was due to an increase in the rate of Ca2+ current inactivation rather than a reduction in peak amplitude.
Our data suggest that compensatory and excess retrieval represent two independent, Ca2+‐regulated mechanisms of rapid membrane internalization in bovine adrenal chromaffin cells. Alternatively, there is a single membrane internalization mechanism that can switch between two distinct modes of behaviour.
Voluntary activation of human elbow flexor muscles during maximal concentric contractions
Authors: Gandevia S. C. , Herbert R. D. , Leeper J. B. 
Published: September 2004

To measure voluntary activation of human elbow flexor muscles during maximal concentric contractions, the twitch interpolation method was modified to enable detection of torque increments evoked by single stimuli during contractions of up to 300 deg s−1. Subjects flexed the elbow to rotate a loaded beam ‘as fast as possible’ (load typically 23–58 N m) from 70 deg below to 70 deg above the horizontal. Electrical stimuli were delivered to biceps brachii when the beam passed through the horizontal. Voluntary activation was estimated from the amplitude of the interpolated twitch, which was expressed as a percentage of the twitch produced by relaxed muscles shortening at the same velocity.
In eleven subjects, the level of voluntary activation during repeated maximal concentric contractions (median 99.4 %) did not differ significantly from that during maximal isometric contractions (98.0 %). Voluntary activation during maximal contractions did not depend on shortening velocity and was the same when tested at two angles 30 deg apart.
To induce fatigue, five subjects repeatedly lifted and lowered a heavy load at about 30 deg s−1, and continued for ten to twelve contractions after they needed assistance to continue lifting. All maintained the capacity to attain maximal levels of activation.
It is concluded that voluntary drive to elbow flexor muscles during maximal concentric contractions is usually maximal or near‐maximal, and that this level of drive can be maintained during development of peripheral fatigue.
Slow recovery of impaired phrenic responses to hypoxia following perinatal hyperoxia in rats
Authors: Ling Liming , Olson E. Burt , Vidruk Edward H. , Mitchell Gordon S. 
Published: September 2004

Previous studies demonstrated that both ventilatory and phrenic nerve responses to acute hypoxia are greatly attenuated in adult rats (3–5 months old) previously exposed to 1 month of perinatal hyperoxia (60 % O2; perinatal treated rats). The present study tested the hypothesis that this functional impairment recovers spontaneously with advancing age in perinatal treated rats.
Hypoxia‐induced chemoreflexes were examined by measuring integrated phrenic responses to strictly controlled isocapnic hypoxia in urethane‐anaesthetized, vagotomized, paralysed and ventilated rats at different ages.
At 50 mmHg Pa,O2 (arterial O2 partial pressure), the hypoxia‐induced increase in minute phrenic activity was significantly attenuated in both 3‐ to 5‐month‐old (166 ± 15 % of baseline) and 6‐month‐old (130 ± 17 %) perinatal treated rats, relative to 3‐ to 6‐month‐old, untreated control rats (279 ± 28 %; both P < 0.05). However, at 40 mmHg Pa,O2, the hypoxic minute phrenic activity response was attenuated only in 3‐ to 5‐month‐old (154 ± 33 %), but not 6‐month‐old (232 ± 33 %) perinatal treated rats versus control rats (293 ± 30 %).
The minute phrenic activity response to hypoxia was not significantly different between geriatric perinatal treated rats (14–15 months) and untreated geriatric control rats at either 50 mmHg (treated: 250 ± 20 %versus control: 274 ± 23 %) or 40 mmHg Pa,O2 (treated: 292 ± 19 %versus control: 315 ± 36 %).
These data suggest that partial spontaneous recovery may occur in 6‐month‐old perinatal treated rats and that full recovery occurs by 15 months of age.
Antioxidant‐oxidant balance in the glomerulus and proximal tubule of the rat kidney
Authors: Gwinner Wilfried , Deters‐Evers Ute , Brandes Ralf P. , Kubat Birgit , Koch Karl‐Martin , Pape Michael , Olbricht Christoph J. 
Published: September 2004

Antioxidant and oxidative enzymes were examined in renal glomeruli and proximal tubules of healthy young rats (10‐12 weeks old), and results were related to the superoxide anion generation of these tissues.
Activities of superoxide dismutases, catalase, and glutathione peroxidase were 3‐ to 6‐fold higher in proximal tubules than in glomeruli. Similarly, enzyme levels and mRNA levels of superoxide dismutases and catalase were significantly higher in proximal tubules.
NADH‐ and NADPH‐dependent oxidase activity and xanthine oxidase activity were not different in glomeruli and proximal tubules.
Measurements with lucigenin‐enhanced chemiluminescence in vital tissues indicated 10‐fold higher rates of superoxide anion in glomeruli than in tubules.
Compared with the young rats, tubules of 8‐month‐old rats had significantly higher superoxide anion rates and lower superoxide dismutase activity, whereas NADH‐ and NADPH‐dependent oxidase activities were unchanged.
We conclude that considerable differences in the antioxidant‐oxidant balance exist between the glomerulus and proximal tubule. Results from experiments using chemiluminescence in vital tissues suggest that changes in the antioxidant‐oxidant balance have an effect on oxygen radical levels. The relevance of the observed differences to glomerular and tubulo‐interstitial disease remains to be determined, but a greater susceptibility of the glomerulus to oxidant stress might be anticipated.
In vivo measurements of the triceps surae complex architecture in man: implications for muscle function
Authors: Maganaris Constantinos N. , Baltzopoulos Vasilios , Sargeant Anthony J. 
Published: September 2004

The objectives of this study were to (1) quantify experimentally in vivo changes in pennation angle, fibre length and muscle thickness in the triceps surae complex in man in response to changes in ankle position and isometric plantarflexion moment and (2) compare changes in the above muscle architectural characteristics occurring in the transition from rest to a given isometric plantarflexion intensity with the estimations of a planimetric muscle model assuming constant thickness and straight muscle fibres.
The gastrocnemius medialis (GM), gastrocnemius lateralis (GL) and soleus (SOL) muscles of six males were scanned with ultrasonography at different sites along and across the muscle belly at rest and during maximum voluntary contraction (MVC) trials at ankle angles of −15 deg (dorsiflexed direction), 0 deg (neutral position), +15 deg (plantarflexed direction) and +30 deg. Additional images were taken at 80, 60, 40 and 20 % of MVC at an ankle angle of 0 deg.
In all three muscles and all scanned sites, as ankle angle increased from −15 to +30 deg, pennation increased (by 6–12 deg, 39–67 %, P < 0.01 at rest and 9–16 deg, 29–43 %, P < 0.01 during MVC) and fibre length decreased (by 15–28 mm, 32–34 %, P < 0.01 at rest and 8–10 mm, 27–30 %, P < 0.05 during MVC). Thickness in GL and SOL increased during MVC compared with rest (by 5–7 mm, 36–47 %, P < 0.01 in GL and 6–7 mm, 38–47 %, P < 0.01 in SOL) while thickness of GM did not differ (P > 0.05) between rest and MVC.
At any given ankle angle the model underestimated changes in GL and SOL occurring in the transition from rest to MVC in pennation angle (by 9–12 deg, 24–38 %, P < 0.01 in GL and 9–14 deg, 25–28 %, P < 0.01 in SOL) and fibre length (by 6–15 mm, 22–39 %, P < 0.01 in GL and 6–8 mm, 23–24 %, P < 0.01 in SOL).
The findings of the study indicate that the mechanical output of muscle as estimated by the model used may be unrealistic due to errors in estimating the changes in muscle architecture during contraction compared with rest.