| 1. |
|
|
| 2. |
- Boedtkjer, D M Briggs, et al.
(author)
-
Vasomotion has chloride-dependency in rat mesenteric small arteries.
- 2008
-
In: Pflügers Archiv : European journal of physiology. - : Springer Science and Business Media LLC. - 0031-6768 .- 1432-2013. ; 457:2, s. 389-404
-
Journal article (peer-reviewed)abstract
- The possibility that Ca(2+)-activated Cl(-) conductances (CaCCs) contribute to oscillations in vascular tone (vasomotion) is tested in isolated mesenteric small arteries from rats where cGMP independent (I (Cl(Ca))) and cGMP-dependent (I (Cl(Ca,cGMP))) chloride conductances are important. The effect of anion substitution and Cl(-) channel blockers on noradrenaline (NA)-stimulated tension in isometrically mounted mesenteric arteries and for chloride conductance of smooth muscle cells isolated from these arteries were assessed electrophysiologically. Cl(-) (o) replacement with aspartate blocked vasomotion while 36mM SCN(-) (o) (substituted for Cl(-)) was sufficient to inhibit vasomotion. Oscillations in tone, membrane potential, and [Ca(2+)](i) disappeared with 36mM SCN(-). DIDS and Zn(2+) blocked I (Cl(Ca,cGMP)) but not I (Cl(Ca)). Vasomotion was not sensitive to DIDS and Zn(2+), and DIDS and Zn(2+) induce vasomotion in arteries without endothelium. The vasomotion in the presence of DIDS and Zn(2+) was sensitive to 36mM SCN(-) (o). The anion substitution data indicate that Cl(-) is crucial for the V (m) and [Ca(2+)](i) oscillations underlying vasomotion. The Cl(-) channel blocker data are consistent with both CaCCs being important.
|
|
| 3. |
- Brismar, Hjalmar, et al.
(author)
-
The role of endocytosis in renal dopamine D1 receptor signaling
- 2006
-
In: Pflügers Archiv. - : Springer Science and Business Media LLC. - 0031-6768 .- 1432-2013. ; 451:6, s. 793-802
-
Journal article (peer-reviewed)abstract
- Desensitization of G-protein-coupled receptors (GPCR) includes receptor endocytosis. This phenomenon is suggested, at least for some receptors, to be associated with receptor resensitization. Here, we examined the role of receptor endocytosis for two different GPCR, the dopamine-1 (D1) receptor and the beta 1-adrenoceptor (beta(1)-AR) in renal tissue. The functional role of receptor endocytosis was examined on Na+, K+-ATPase activity in microdissected proximal tubules from rat kidney. The spatial regulation of endogenous D1 receptors and beta(1)-AR was examined by confocal microscopy techniques in LLCPK cells. Phenylarsine oxide (PAO) an endocytosis inhibitor, attenuated isoproterenol-induced decrease in Na+, K+-ATPase activity but had no such effect on dopamine-induced decrease in Na+, K+-ATPase activity. We have previously shown that isoproterenol sensitizes the renal dopamine system, by recruiting silent D1 receptors from the interior of the cell towards the plasma membrane. This effect was attenuated by PAO as well as by cytochalasin D while these substances had no effect on dopamine-induced D1 receptor recruitment. The beta(1)-AR was localized to the plasma membrane in control cells. Isoproterenol induced a rapid internalization of the beta(1)-AR; which was prevented by PAO. The results suggest that endocytosis of beta(1)-AR in renal proximal tubular cells is an important step in signal generation, while endocytosis of proximal tubular D1 receptor is not.
|
|
| 4. |
|
|
| 5. |
- Jiang, Chonghe, et al.
(author)
-
Bladder cooling reflex and external urethral sphincter activity in the anesthetized and awake guinea pig
- 2008
-
In: Pflügers Archiv. - : Springer Science and Business Media LLC. - 0031-6768 .- 1432-2013. ; 457:1, s. 61-66
-
Journal article (peer-reviewed)abstract
- A spinal bladder cooling reflex, triggered by cold receptors of transient receptor potential melastatin type in the bladder wall, has been identified in several mammals, including man. This reflex and its influence on the external urethral sphincter were further characterized in the urethane anesthetized and awake guinea pigs. A total of 214 bladder infusions were performed in the 12 animals. Compared to controls, cold fluid induced a significant decrease in the threshold volume for reflex bladder contractions (median 82%, p<0.01). Menthol induced a further decrease (median 50%), signifying a bladder cooling reflex. Detrusor-sphincter activities were dyssynergic during voidings triggered by cold or menthol infusions but were coordinated during control infusions. The bladder cooling reflex was suppressed and the sphincter activity synergic following cold infusions in the awake state. Thus, the bladder cooling reflex is under the active descending inhibitory control in intact, awake animals. © 2008 Springer-Verlag.
|
|
| 6. |
- Kadi, Fawzi, et al.
(author)
-
The behaviour of satellite cells in response to exercise : what have we learned from human studies?
- 2005
-
In: Pflügers Archiv. - : Springer Science and Business Media LLC. - 0031-6768 .- 1432-2013. ; 451:2, s. 319-327
-
Journal article (other academic/artistic)abstract
- Understanding the complex role played by satellite cells in the adaptive response to exercise in human skeletal muscle has just begun. The development of reliable markers for the identification of satellite cell status (quiescence/activation/proliferation) is an important step towards the understanding of satellite cell behaviour in exercised human muscles. It is hypothesised currently that exercise in humans can induce (1) the activation of satellite cells without proliferation, (2) proliferation and withdrawal from differentiation, (3) proliferation and differentiation to provide myonuclei and (4) proliferation and differentiation to generate new muscle fibres or to repair segmental fibre injuries. In humans, the satellite cell pool can increase as early as 4 days following a single bout of exercise and is maintained at higher level following several weeks of training. Cessation of training is associated with a gradual reduction of the previously enhanced satellite cell pool. In the elderly, training counteracts the normal decline in satellite cell number seen with ageing. When the transcriptional activity of existing myonuclei reaches its maximum, daughter cells generated by satellite cell proliferation are involved in protein synthesis by enhancing the number of nuclear domains. Clearly, delineating the events and the mechanisms behind the activation of satellite cells both under physiological and pathological conditions in human skeletal muscles remains an important challenge.
|
|
| 7. |
- Marx, James O, et al.
(author)
-
Scaling of skeletal muscle shortening velocity in mammals representing a 100,000-fold difference in body size
- 2006
-
In: Pflügers Archiv. - Heidelberg : Springer. - 0031-6768 .- 1432-2013. ; 452:2, s. 222-230:452, s. 222-230
-
Journal article (peer-reviewed)abstract
- To fully understand the effect of scaling on skeletal muscle shortening velocity (V 0), it is important to know which phenotypic characteristics drive the changes between species. The purpose of the current investigation was to compare the effects of body mass and femur length, as an estimate of total limb length, on V 0 in species that cover a 100,000-fold range of body masses. Using the slack test procedure, V 0 was determined for fibers expressing types I and IIa myosin heavy chain (MyHC) isoforms in the mouse, rat, dog, human, horse, and rhinoceros under identical experimental conditions. A significant scaling effect on V 0 was detected when compared to body mass (type I fibers, r=0.95, p<0.01; type IIa fibers, r=0.83, p<0.05). However, the horse's V 0 for both fiber types was faster than the human's, despite having a 5-fold greater body mass than the human. When V 0 was scaled vs limb length, the strength of the relationships improved in fibers expressing both types I and IIa MyHC (r=0.98, p<0.001, and r=0.89, p<0.05, respectively) and scaled with the expected relationship, with the species with the shorter femur, the horse, having the faster V 0. A similar effect can be seen with stride frequency scaling more closely with limb length than body mass. These results suggest that limb length, not body mass, is a more relevant factor driving the scaling effect on skeletal muscle shortening velocity.
|
|
| 8. |
- Norman, Holly, et al.
(author)
-
Impact of post-synaptic block of neuromuscular transmission, muscle unloading and mechanical ventilation on skeletal muscle protein and mRNA expression
- 2006
-
In: Pflügers Archiv. - : Springer Science and Business Media LLC. - 0031-6768 .- 1432-2013. ; 453:1, s. 53-66
-
Journal article (peer-reviewed)abstract
- To analyse mechanisms of muscle wasting in intensive care unit patients, we developed an experimental model where rats were pharmacologically paralysed by post-synaptic block of neuromuscular transmission (NMB) and mechanically ventilated for 9 2 days. Specific interest was focused on the effects on protein and mRNA expression of sarcomeric proteins, i.e., myosin heavy chain (MyHC), actin, myosin-binding protein C (MyBP-C) and myosin-binding protein H (MyBP-H) in fast- and slow-twitch limb, respiratory and masticatory muscles. Muscle-specific differences were observed in response to NMB at both the protein and mRNA levels. At the protein level, a decreased MyHC-to-actin ratio was observed in all muscles excluding the diaphragm, whereas at the mRNA level a decreased expression of the dominating MyHC isoform(s) was observed in the hind limb and intercostal muscles, but not in the diaphragm and masseter muscles. MyBP-C mRNA expression was decreased in the limb muscles, but it otherwise remained unaffected. MyBP-H conversely increased in all muscles. Furthermore, we found myofibrillar protein and mRNA expression to be affected differently when comparing NMB; animals with peripherally denervated (DEN) ambulatory rats. We report that NMB; has both a larger and different impact on muscle, at the protein and mRNA levels, than DEN has.
|
|
| 9. |
- Ochala, Julien, et al.
(author)
-
Single skeletal muscle fiber behavior after a quick stretch in young and older men : a possible explanation of the relative preservation of eccentric force in old age
- 2006
-
In: Pflügers Archiv. - : Springer Science and Business Media LLC. - 0031-6768 .- 1432-2013. ; 452:4, s. 464-470
-
Journal article (peer-reviewed)abstract
- The origins of the smaller age-related decrease in eccentric force compared to isometric and concentric conditions in vivo remain unclear. Could this originate from contractile elements of muscle cells? The main intent of the current investigation was to assess the force behavior of muscle cells with aging, during lengthening. Chemically skinned single muscle fibers (n=235) from m. vastus lateralis of six young (mean age 31.6 years) and six older men (mean age 66.1 years) were maximally activated with pCa 4.5 at 15 degrees C. Maximal isometric force and cross-sectional area were measured allowing the calculation of the tension (T-0). A quick stretch (2 nm per half-sarcomere length) was applied and caused an immediate increase in tension followed by a decrease and a secondary delayed and transient rise in tension (phase 3); finally, the tension recovered a steady state value (phase 4). The tension enhancements during phase 3 (Delta T (3)) and phase 4 (Delta T (4)) were evaluated. The myosin heavy-chain isoform composition of each single fiber was determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Delta T (3) and Delta T (4) were preserved in older men for both type I and IIa fibers despite a reduction in T-0. Therefore, the age-related preservation of the tension increments after a quick stretch in single muscle fibers could explain in part the smaller decrease in force during eccentric contractions compared to isometric and concentric conditions in vivo with aging usually observed.
|
|
| 10. |
- Pantazis, Antonios, 1982-, et al.
(author)
-
The Effect of Neuronal Morphology and Membrane-permeant Weak Acid and Base on the Dissipation of Depolarization-induced pH Gradients in Snail Neurons
- 2006
-
In: Pflügers Archiv. - : Springer. - 0031-6768 .- 1432-2013. ; 452:2, s. 175-187
-
Journal article (peer-reviewed)abstract
- Neuronal depolarization causes larger intracellular pH (pHi) shifts in axonal and dendritic regions than in the cell body. In this paper, we present evidence relating the time for collapse of these gradients to neuronal morphology. We have used ratiometric pHi measurements using 8-hydroxypyrene-1,3,6-trisulfonic acid (HPTS) in whole-cell patch-clamped snail neurons to study the collapse of longitudinal pH gradients. Using depolarization to open voltage-gated proton channels, we produced alkaline pHi microdomains. In the absence of added mobile buffers, facilitated H+ diffusion down the length of the axon plays a critical role in determining pHi microdomain lifetime, with axons of ∼100 μm allowing pH differences to be maintained for >60 s. An application of mobile, membrane-permeant pH buffers accelerated the collapse of the alkaline-pH gradients but, even at 30 mM, was unable to abolish them. Modeling of the pHi dynamics showed that both the relatively weak effect of the weak acid/base on the peak size of the pH gradient and the accelerated collapse of the pH gradient could be due to the time taken for equilibration of the weak acid and base across the cell. We propose that appropriate weak acid/base mixes may provide a simple method for studying the role of local pHi signals without perturbing steady-state pHi. Furthermore, an extrapolation of our in vitro data to longer and thinner neuronal structures found in the mammalian nervous system suggests that dendritic and axonal pHi are likely to be dominated by local pHi-regulating mechanisms rather than simply following the soma pHi.
|
|
