bluuebunny/crossref_metadata_2025_split huggingface dataset:
Adenosine formation in contracting primary rat skeletal muscle cells and endothelial cells in culture
Authors: Hellsten Y. , Frandsen U. 
Published: September 2004

The present study examined the capacity for adenosine formation, uptake and metabolism in contracting primary rat muscle cells and in microvascular endothelial cells in culture.
Strong and moderate electrical simulation of skeletal muscle cells led to a significantly greater increase in the extracellular adenosine concentration (421 ± 91 and 235 ± 30 nmol (g protein)−1, respectively; P < 0.05) compared with non‐stimulated muscle cells (161 ± 20 nmol (g protein)−1). The ATP concentration was lower (18%; P < 0.05) in the intensely contracted, but not in the moderately contracted muscle cells.
Addition of microvascular endothelial cells to the cultured skeletal muscle cells enhanced the contraction‐induced accumulation of extracellular adenosine P < 0.05), whereas endothelial cells in culture alone did not cause extracellular accumulation of adenosine.
Skeletal muscle cells were found to have ecto‐forms of several enzymes involved in nucleotide metabolism, including ATPases capable of converting extracellular ATP to ADP and AMP.
Adenosine added to the cell medium was taken up by muscle cells and incorporated into the adenine nucleotide pool so that after 30 min of incubation, over 95% of the adenosine label was present in ATP, ADP and AMP. A similar extent of incorporation of adenosine into the nucleotide pool was evident in the endothelial cells.
The present data suggest that contracting muscle cells induce an elevation in the extracellular adenosine concentration. Addition of endothelial cells to muscle cells enhances the contraction‐induced formation of adenosine. Adenosine taken up by muscle and endothelial cells from the extracellular space is not likely to be used for storage in intracellular pools, but may serve to regulate muscle extracellular adenosine levels.
Firing pattern of type‐identified wrist extensor motor units during wrist extension and hand clenching in humans
Authors: Sturm Hendrik , Schmied Annie , Vedel Jean‐Pierre , Pagni Simone 
Published: September 2004

Single motor unit activity was investigated in the extensor carpi radialis muscles during voluntary isometric contraction involving either the coactivation of the wrist agonist extensor muscles (wrist extension) or the coactivation of the wrist and finger antagonist extensor and flexor muscles (hand clenching).
The motor units were found to be activated at a similar level of motoneurone pool drive during both wrist extension and hand clenching, as indicated by the fact that the EMG activity at which they were recruited was practically the same in both cases (mean ±s.d.: 20 ± 26 and 21 ± 25 mV, respectively). In addition, the net excitatory drive exerted on the motoneurones, as assessed from the mean interspike intervals, did not differ significantly between the two tasks (mean ±s.d.: 104.57 ± 17.24 and 103.01 ± 16.26 ms, for wrist extension and hand clenching, respectively).
However, the discharge variability, in terms of the coefficient of variation of the interspike intervals, was slightly but significantly greater during hand clenching than during wrist extension (0.213 ± 0.049 and 0.198 ± 0.045, respectively). This increase involved all types of motor units, regardless of their contractile force.
We suggest that the greater motoneurone discharge variability observed during hand clenching may be attributable to an increase in the synaptic noise. This increase might be due to the activation of numerous afferent pathways mediating reciprocal interactions between antagonist motoneurone pools, as well as to the activation of hand cutaneous receptors that play a major role in the regulation of handling and gripping motor activities.
Luminal and basolateral endothelin inhibit chloride reabsorption in the mouse thick ascending limb via a Ca2+‐Independent Pathway
Authors: de Jesus Ferreira Marie Celeste , Bailly Claire 
Published: September 2004

The recent localization of endothelin synthesis and receptors in the thick ascending limb (TAL) prompted us to investigate a possible autocrine and/or paracrine effect of this agent. The net chloride flux (JCl) has been determined in isolated cortical and medullary TALs by the in vitro microperfusion technique.
In both segments, endothelin 1 (ET‐1) at 10−8m in the bath significantly decreased JCl, an effect which was partially reversible and observed at concentrations equal to or greater than 10−13m.
This (JCl inhibition (by 33.9 ± 3.2%) was blocked by BQ788 and was also observed with sarafotoxin 6C and ET‐3, indicating that endothelin receptor B (ETB) are present in TAL.
ET‐1 did not affect cAMP content under basal or hormone‐stimulated conditions. The presence of a prostaglandin synthesis inhibitor also did not prevent the ET‐1 action on JCl.
The ET‐1‐induced inhibition of JCl was prevented by protein kinase C inhibitors (staurosporine or GF 109203) and was reproduced by diacylglycerol analogues (OAG and DiC8). However, ET‐1 failed to increase intracellular Ca2+ concentration.
Addition of ET‐1 or ET‐3 to the apical surface induced a decrease of JCl through ETB receptors, an effect which was not additive with that induced by basolateral ET‐1, and was not concomitant with an increase in intracellular Ca2+ concentration.
It is concluded that the basolateral and luminal inhibitions of JCl by ET‐1 in TAL, through ETB receptors, is mediated by a protein kinase C activation which is independent of intracellular Ca2+ increase.
The effects of neonatal median nerve injury on the responsiveness of Tactile neurones within the cuneate nucleus of the cat
Authors: Murray G. M. , Taub D. R. , Mackie P. D. , Zhang H. Q. , Ghosh S. , Rowe M. J. 
Published: September 2004

The capacity of cuneate neurones to attain normal functional properties following neonatal median nerve injury was investigated with single neurone recording in anaesthetized cats, 12–24 months subsequent to a controlled crush injury. Effectiveness of the peripheral nerve injury was confirmed by the abolition of the median nerve compound action potential following the crush.
Cuneate recording was carried out after denervation of the forearm, apart from the median nerve, to ensure that neurones studied had receptive fields within the distribution zone of the regenerated median nerve. Controlled and reproducible tactile stimuli were used to evaluate the functional capacities of neurones to determine whether they were consistent with those reported earlier for cuneate neurones in cats that had normal peripheral nerve development.
Twenty‐two cuneate neurones with well‐defined tactile receptive fields within the distribution zone of the regenerated median nerve were classified according to their adaptation characteristics and functional properties. Slowly adapting neurones responded throughout static skin indentations and had graded and approximately linear stimulus–response relations over indentation ranges up to 1.5 mm. Rapidly adapting neurones responded to the dynamic phases of skin indentations and could be divided into two broad classes, one most sensitive to vibrotactile stimuli at 200–400 Hz which appeared to receive a predominant input from Pacinian corpuscle receptors, and a non‐Pacinian group that included neurones most sensitive to skin vibration at 5–50 Hz which appeared to receive glabrous skin input from the rapidly adapting class of afferent fibres.
Based on the stimulus‐response relations and on measures of phase locking in the responses to vibrotactile stimuli, it appears that the functional properties of cuneate neurones activated from the field of a regenerated median nerve subsequent to a neonatal nerve crush injury were consistent with those reported previously for ‘control’ cuneate neurones. The results indicate that cuneate neurones can acquire normal tactile coding capacities despite the disruption caused by prior crush injury to their peripheral nerve source.
Quantitative analysis of cuneate neurone responsiveness in the cat in association with reversible, partial deafferentation
Authors: Zhang S. P. , Rowe M. J. 
Published: September 2004

Partial deafferentation, based on peripheral nerve section or local anaesthetic blockade, has been reported to induce both immediate loss of responsiveness and/or immediate reorganization in receptive fields of neurones in the somatosensory system. In the present study, in anaesthetized cats, we have used a rapid, reversible deafferentation procedure based on cold block of the median nerve in order to evaluate quantitatively the response characteristics of cuneate neurones (n= 39) before, during and after partial deafferentation.
The first hypothesis tested was that cuneate neurones with input from ulnar or superficial radial nerve fields in the vicinity of the median nerve field should undergo, in association with median nerve blockade, an increased level of responsiveness to tactile stimuli within the ulnar or radial nerve zone, and an expansion of their cutaneous receptive fields. However, among eighteen cuneate neurones of this type, there was no evidence for any systematic enhancement of responsiveness nor, in at least sixteen of the eighteen neurones, any evidence for receptive field expansion.
The second hypothesis tested was that cuneate neurones whose input came from both the median nerve and another peripheral nerve source should undergo, in association with median nerve blockade, an increase in responsiveness to the remaining input and an expansion of the receptive field into the field of that remaining nerve source. However, in none of thirteen neurones of this type tested was there evidence of such a change.
The third hypothesis was that cuneate neurones whose ‘control’ receptive fields werewithin the median nerve zone of deafferentation should show an emergence of novel receptive fields and responsiveness from areas around the field of innervation of the median nerve. However, in none of eight neurones of this type was there evidence for such changes in adjacent skin areas.
In conclusion, with the use of cold block of the median nerve for partial deaffferentation, the present study has confirmed previous findings of denervation‐related loss of responsiveness in dorsal column nuclei neurones. The conflicting findings in studies of central nervous system plasticity indicate the need to understand better factors that do and do not lead to acute central changes.
Hypoxic response of hypoglossal motoneurones in the in vivo cat
Authors: Pierrefiche O. , Bischoff A. M. , Richter D. W. , Spyer K. M. 
Published: September 2004

In current and voltage clamp, the effects of hypoxia were studied on resting and synaptic properties of hypoglossal motoneurones in barbiturate‐anaesthetized adult cats.
Twenty‐nine hypoglossal motoneurones with a mean membrane potential of −55 mV responded rapidly to acute hypoxia with a persistent membrane depolarization of about +17 mV. This depolarization correlated with the development of a persistent inward current of 0.3 nA at holding potentials close to resting membrane potential.
Superior laryngeal nerve (SLN) stimulation‐evoked EPSUPs were reduced in amplitude by, on average, 46%, while IPSUP amplitude was reduced by 31 %. SLN stimulation‐evoked EPSCs were reduced by 50–70%.
Extracellular application of adenosine (10 mm) hyperpolarized hypoglossal motoneurones by, on average, 5.6 mV, from a control value of –62 mV. SLN stimulation‐evoked EPSUPs decreased by 18% and IPSUPs decreased by 46% during adenosine application.
Extracellular application of the KATP channel blocker glibenclamide led to a blockade of a persistent outward current and a significant increase of SLN stimulation‐evoked EPSCs.
We conclude that hypoglossal motoneurones have a very low tolerance to hypoxia. They appear to be under metabolic stress even in normoxia and their capacity to activate protective potassium currents is limited when compared with other brainstem neurones. This may help to explain the rapid disturbance of hypoglossal function during energy depletion.
Cholecystokinin (CCK) regulates somatostatin secretion through both the CCK‐A and CCK‐B/gastrin receptors in sheep
Authors: Zavros Yana , Shulkes Arthur 
Published: September 2004

Cholecystokinin (CCK) and gastrin both stimulate gastric somatostatin (SOM) secretion in vitro and thus have the potential to modulate their direct effects on the parietal cell. However, the relative potencies and the mechanisms of action of CCK and gastrin on SOM secretion in vivo have not been determined.
The objectives of the present study were to compare the in vivo potencies of the sulphated (s) and non‐sulphated (ns) forms of gastrin heptadecapeptide (G‐17) and CCK octapeptide (CCK‐8) on SOM secretion, and to determine the nature of the receptors involved by repeating the studies in the presence of the CCK‐A and CCK‐B/gastrin receptor antagonists L‐364,718 and L‐365,260, respectively. All experiments were performed in the chronically cannulated sheep.
Dose–response experiments revealed the following potencies for SOM secretion: G‐17s = CCK‐8s > G‐17ns ≫ CCK‐8ns. However, based on the plasma levels achieved and a higher metabolic clearance rate (MCR) for CCK, CCK‐8s was the most potent.
Both the CCK‐A and CCK‐B/gastrin receptor antagonists suppressed CCK‐8s‐stimulated SOM output. In contrast, G‐17s‐stimulated SOM output was inhibited by only the CCK‐B/gastrin receptor antagonist.
Both receptor antagonists increased basal plasma gastrin and CCK levels.
The predominant circulating SOM molecular form after both gastrin and CCK stimulation was SOM‐14.
In conclusion, the sulphated forms of CCK and gastrin are more potent than the non‐sulphated forms. Despite sharing a common biologically active carboxy terminus, CCK stimulates SOM secretion by both the CCK‐A and CCK‐B/gastrin receptors, while gastrin acts via the CCK‐B/gastrin receptor alone. These findings explain in part why CCK is a net inhibitor of gastric acid secretion in vivo.
Abnormal regional blood flow responses during and after exercise in human sympathetic denervation
Authors: Puvi‐Rajasingham Sharmini , Smith Gareth D. P. , Akinola Adeola , Mathias Christopher J. 
Published: September 2004

Blood pressure, superior mesenteric artery (SMA) and skeletal muscle blood flow, cardiac index (CI) and systemic vascular resistance responses to supine leg exercise were measured in six age‐matched normal subjects (controls) and in eleven subjects with sympathetic denervation due to primary autonomic failure (AF).
During exercise, blood pressure rose in controls but fell markedly in AF. After exercise, blood pressure rapidly returned to baseline in controls but remained low in AF. During exercise, systemic vascular resistance fell in controls and AF but tended to fall further in AF and remained low post exercise. CI increased similarly in controls and AF.
During exercise, SMA blood flow fell similarly in controls and AF, but the fall initially was slower in AF; recovery was more rapid post exercise in controls. SMA vascular resistance tended to rise less and more slowly in AF and remained elevated post exercise.
Forearm muscle (FM) blood flow and FM vascular resistance did not change from resting values in controls or AF post exercise. After exercise, leg muscle (LM) blood flow rose and LM vascular resistance fell equally in both groups although LM blood flow remained elevated, 10 min post exercise in AF.
In sympathetically denervated humans, increased blood flow (due to excessive vasodilatation, lack of sympathetic restraint, or both) in leg muscle during and after exercise in combination with impaired splanchnic vasoconstriction in the early stages of exercise may have contributed to exercise‐induced hypotension.
Variation of electroencephalographic activity during non‐rapid eye movement and rapid eye movement sleep with phase of circadian melatonin rhythm in humans
Authors: Dijk Derk‐Jan , Shanahan Theresa L. , Duffy Jeanne F. , Ronda Joseph M. , Czeisler Charles A. 
Published: September 2004

The circadian pacemaker regulates the timing, structure and consolidation of human sleep. The extent to which this pacemaker affects electroencephalographic (EEG) activity during sleep remains unclear.
To investigate this, a total of 1.22 million power spectra were computed from EEGs recorded in seven men (total, 146 sleep episodes; 9 h 20 min each) who participated in a one‐month‐long protocol in which the sleep–wake cycle was desynchronized from the rhythm of plasma melatonin, which is driven by the circadian pacemaker.
In rapid eye movement (REM) sleep a small circadian variation in EEG activity was observed. The nadir of the circadian rhythm of α‐activity (8.25–10.5 Hz) coincided with the end of the interval during which plasma melatonin values were high, i.e. close to the crest of the REM sleep rhythm.
In non‐REM sleep, variation in EEG activity between 0.25 and 11.5Hz was primarily dependent on prior sleep time and only slightly affected by circadian phase, such that the lowest values coincided with the phase of melatonin secretion.
In the frequency range of sleep spindles, high‐amplitude circadian rhythms with opposite phase positions relative to the melatonin rhythm were observed. Low‐frequency sleep spindle activity (12.25–13.0 Hz) reached its crest and high‐frequency sleep spindle activity (14.25–15.5Hz) reached its nadir when sleep coincided with the phase of melatonin secretion.
These data indicate that the circadian pacemaker induces changes in EEG activity during REM and non‐REM sleep. The changes in non‐REM sleep EEG spectra are dissimilar from the spectral changes induced by sleep deprivation and exhibit a close temporal association with the melatonin rhythm and the endogenous circadian phase of sleep consolidation.
Evidence showing that β‐adrenoceptor subtype responsible for the relaxation induced by isoprenaline is principally β2 but not β1 in guinea‐pig tracheal smooth muscle
Authors: Tanaka Y. , Yamashita Y. , Horinouchi T. , Yamaki F. , Koike K. 
Published: September 2004

Summary 1 The present study was carried out to pharmacologically identify the β‐adrenoceptor subtype that mediates isoprenaline‐elicited relaxation in the isolated guinea‐pig tracheal smooth muscle, to answer the question whether it is β1‐ or β2‐subtype? 2 Isoprenaline as well as salbutamol, a well‐known β2‐selective adrenoceptor agonist, produced a concentration‐dependent relaxation with a pD2 value of 8.12 vs. 7.54 for salbutamol. 3 Isoprenaline‐elicited relaxation was not affected by β1‐selective antagonists, atenolol and CGP‐20,712A, within the concentration ranges supposed to antagonize β1‐subtype: atenolol, ≤10−6 m; CGP‐20,712A, ≤10−8 m. 4 By contrast, the concentration–response curves for isoprenaline as well as salbutamol were shifted rightwards in a competitive fashion by atenolol at the concentrations ≥3 × 10−6 m. However, pA2 values of atenolol against isoprenaline (5.86) and salbutamol (5.71) were consistent with the value corresponding to β2‐ but not to β1‐subtype (around 7.00), and these values were not significantly different from each other. 5 Competitive antagonism of the relaxations to isoprenaline and salbutamol were also obtained with β2‐selective antagonists, butoxamine and ICI‐118,551. Against isoprenaline and salbutamol, the pA2 values of butoxamine (6.51 vs. 6.81) and ICI‐118,551 (8.83 vs. 8.90) were substantially identical. Thus the primary mediation of β2‐receptor in the relaxations was strongly supported. 6 The present findings provide evidence that the β‐adrenoceptor which mediates isoprenaline‐elicited relaxation of guinea‐pig tracheal smooth muscle is essentially β2‐ but not β1‐subtype. The present study also indicates the importance of using multiple receptor antagonists with different pA2 values to pharmacologically identify the responsible receptor subtype in smooth muscle mechanical responses.
Functional alterations of mesenteric vascular bed, vas deferens and intestinal tracts in a rat hindlimb unloading model of microgravity
Authors: De Salvatore G. , Desaphy J.‐F. , Piepoli A. L. , Natale L. , De Salvia M. A. , Mitolo C. I. , Renna G. , Conte‐Camerino D. , Mitolo‐Chieppa D. 
Published: September 2004

Summary 1 Prolonged bed rest or exposure to microgravity may cause several alterations in autonomic nervous system response (ANSR). 2 Hindlimb unloading (HU) rats were used as an animal model of simulated microgravity to investigate ANSR changes. The experiments were carried out to investigate the effects of simulated microgravity on the autonomic nervous response of the perfused mesenteric vascular bed (MVB), vas deferens and the colon and duodenum from 2‐week HU rats. 3 In MVB preparations of HU rats, the frequency‐dependent increases in perfusion pressure with perivascular nerve stimulation (PNS; 8–40 Hz) were inhibited, whereas the noradrenaline (NA) concentration‐dependent (1–100 μm) perfusion pressure increases were potentiated. The latter most probably reflected up‐regulation of α‐adrenergic receptor function. Relaxant responses of NA‐precontracted MVB to PNS (4–30 Hz) or isoprenaline were not different between control and HU preparations, while vasodilation induced by the endothelial agonist ACh was reduced. 4 Transmural stimulation (2–40 Hz) induced frequency‐dependent twitches of the vas deferens which were reduced in vas deferens of HU rats, while the sensitivity to NA‐induced contraction was significantly increased. 5 In the gastroenteric system of HU rat, direct contractile responses to carbachol or tachykinin as well as relaxant or contractile responses to nervous stimulation appeared unchanged both in the proximal colon rings and in duodenal longitudinal strips. 6 In conclusion, HU treatment affects peripheral tissues in which the main contractile mediators are the adrenergic ones such as resistance vessels and vas deferens, probably by reducing the release of neuromediator. This study validates NA signalling impairment as a widespread process in microgravity, which may most dramatically result in the clinical phenotype of orthostatic intolerance.
Factors predicting sexual relationships in older people: an Australian study
Authors: Minichiello Victor , Plummer David , Loxton Deborah 
Published: September 2004

Objectives:  Sexuality in later life is now recognised to be an important issue. The present study identified the factors that predict sexual relationships and changes in sexual activity in a sample of 844 older persons living in Melbourne, Australia, who returned a self‐completed questionnaire. Method:  The variables included in the two models that predicted sexual relationship status and changes in sexual activity were: sex, age, marital status, general health, incontinence, satisfaction with physical condition, knowledge of sexual issues, change in sexual interest, perceptions of sex as an important factor in general well‐being, and number of sexual partners. Results and Conclusion:  Logistic regression analysis revealed that the variables used in the model produced correct prediction rates for 84% of respondents not in a sexual relationship, and 85% for those in a sexual relationship. Age, marital status, incontinence, satisfaction with physical condition, sexual knowledge, perceptions of sex as important to well‐being, and number of sexual partners were significantly related to sexual relationship status. The present study discusses how these findings can further inform research and be used to inform our knowledge on sexuality in later life.