Acta Physiologica (ACTA PHYSIOL)

Publications in this journal

• Article: Evaluation of the mechanism of action of ERβ subtypes in health and disease

  A. COLCIAGO, O. MORNATI, L. CASATI, F. CELOTTI, P. NEGRI CESI
  Acta Physiologica 01/2011; 203(688):P1.24.
• Article: The effect of adenosine and atropine combination on the arrhythmia that has occurredfollowing coronary occlusion in rats

  Yaşar S, Kaya T, Hayriye O, Bozdoğan Ö
  Acta Physiologica 01/2011; 203((Supplement 686)):PC062.
• Article: Localization of gat1 protein in testes of stress-exposed rats: an immunohistochemical study

  Demirci T, Ozbek E
  Acta Physiologica 01/2011; 203(Suppl.):686.
• Article: EPIGENOME AND ENVIRONMENT: EFFECTS OF A PCB EXPOSURE ON EPIGENOME DURING EARLY DEVELOPMENT IN THE RAT

  R. Sendra, D. Huertas, M. Esteller, O. Mornati, F. Celotti, A. Colciago, P. Negri-Cesi, L. Casati
  Acta Physiologica 01/2010; 200(S681):P124.
• Article: Epigenetic effects of a PCB exposure during early development in the rat.

  Casati L, Sendra R, Colciago A, Huertas Ruz D, Celotti F, Esteller M, Negri-Cesi P
  Acta Physiologica 01/2009; 197(S672).
• Article: Platelet-enriched plasma (PRP) and cytoskeleton rearrangement in human osteoblasts.

  Casati L, Colciago A, Castano P, Mornati O, Celotti F, Negri-Cesi P
  Acta Physiologica 01/2008; 194(S665):P33.
• Article: iNOS-derived NO depresses Connexin 43 in the mouse with infarct-induced heart failure

  Patience E. M. Jackson, Qingping Feng, Douglas L. Jones
  Acta Physiologica 01/2008; 194:23-33.
• Article: Peroxisome proliferator-activated receptors and inflammation: take it to heart.

  P J H Smeets, A Planavila, G J van der Vusse, M van Bilsen
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  ABSTRACT: Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors acting as key regulators of lipid metabolism as well as modulators of inflammation. The role of PPARalpha and PPARgamma in cardiac ischaemia-reperfusion injury, infarct healing and hypertrophy is the subject of intense research. Due to the later development of PPARdelta-specific ligands, the role of this PPAR isoform in cardiac disease remains to be established. Although many studies point to salutatory effects of PPAR ligands in cardiac disease, the exact molecular mechanism is still largely unsolved. Both the metabolic (via transactivation) and the more recently discovered anti-inflammatory (via transrepression) effects of PPARs are likely to play a role. In this review the reported, and sometimes contradictory, effects of PPAR ligands on ischaemia-reperfusion, infarct healing and cardiac hypertrophy are critically evaluated. In particular the role of inflammation in these disease processes, the ability of PPARs to interfere with pro-inflammatory processes, and the mechanisms of transrepression are discussed. Currently, the significance of PPARs as therapeutic targets in cardiovascular disease is receiving widespread attention. Accordingly, detailed understanding of the mechanisms controlling the activity of these nuclear hormone receptors is essential.
  Acta Physiologica 12/2007; 191(3):171-88.
• Article: Fish cardiac sodium channels are tetrodotoxin sensitive.

  J Haverinen, M Hassinen, M Vornanen
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  ABSTRACT: Sodium current (I(Na)) of the mammalian heart is resistant to tetrodotoxin (TTX) due to low TTX affinity of the cardiac sodium channel (Na(v)) isoform Na(v)1.5. To test applicability of this finding to other vertebrates, TTX sensitivity of the fish cardiac I(Na) and its molecular identity were examined. Molecular cloning and whole-cell patch-clamp were used to examine alpha-subunit composition and TTX inhibition of the rainbow trout (Oncorhynchus mykiss) cardiac Na(v) respectively. I(Na) of the trout heart is about 1000 times more sensitive to TTX (IC50 = 1.8-2 nm) than the mammalian cardiac I(Na) and it is produced by three Na(v)alpha-subunits which are orthologs to mammalian skeletal muscle Na(v)1.4, cardiac Na(v)1.5 and peripheral nervous system Na(v)1.6 isoforms respectively. Oncorhynchus mykiss (om) omNa(v)1.4a is the predominant isoform of the trout heart accounting for over 80% of the Na(v) transcripts, while omNa(v)1.5a forms about 18% and omNa(v)1.6a only 0.1% of the transcripts. OmNa(v)1.4a and omNa(v)1.6a have aromatic amino acids, phenylalanine and tyrosine, respectively, in the critical position 401 of the TTX binding site of the domain I, which confers their high TTX sensitivity. More surprisingly, omNa(v)1.5a also has an aromatic tyrosine in this position, instead of the cysteine of the mammalian TTX-resistant Na(v)1.5. The ortholog of the mammalian skeletal muscle isoform, omNa(v)1.4a, is the predominant Na(v)alpha-subunit in the trout heart, and all trout cardiac isoforms have an aromatic residue in position 401 rendering the fish cardiac I(Na) highly sensitive to TTX.
  Acta Physiologica 12/2007; 191(3):197-204.
• Article: Lacking deoxygenation-linked interaction between cytoplasmic domain of band 3 and HbF from fetal red blood cells.

  R E Weber
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  ABSTRACT: Several of the red blood cell's metabolic and membrane functions display dependence on haemoglobin oxygenation. In adult human red cells, the increased glycolytic rate at low O2 tension results from binding of deoxygenated HbA at negatively charged, N-terminal, cytoplasmic domain of the membrane protein band 3, which liberates glycolytic enzymes from this site. This study aims to investigate the role of fetal HbF (that has lower anion-binding capacity than HbA) in fetal red cells (that are subjected to low O2 tensions), and to elucidate possible linkage (e.g. via the major red cell membrane organising centre, band 3) between the individual oxygenation-linked reactions encountered in red cells. The interaction between band 3 and Hb is analysed in terms of the effects, measured under different conditions, of a 10-mer peptide that corresponds to the N-terminus of human band 3 protein, on the oxygenation reaction of HbF and HbA, isolated from umbilical chord red cells. Contrasting with the unequivocal interaction of the peptide with HbA that with fetal HbF is weak, and annihilated in the presence of autochthonous red cell O2 affinity modulators (chloride and organic phosphates). The data indicate that HbF does not function as a transducer mediating O2 dependence of glycolysis in fetal red cells, in accordance with the different O2 and metabolic profiles compared to those in HbA-bearing adult red cells. In conjunction with the previously discovered O2 dependence of K+ transport in HbF-rich fetal cells, they moreover argue against linkage between different, physiologically relevant, O2-dependent red cell functions.
  Acta Physiologica 12/2007; 191(3):247-52.
• Article: Control of the triceps surae during the postural sway of quiet standing.

  C D Tokuno, M G Carpenter, A Thorstensson, S J Garland, A G Cresswell
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  ABSTRACT: The present study investigated how the triceps surae are controlled at the spinal level during the naturally occurring postural sway of quiet standing. Subjects stood on a force platform as electrical stimuli were applied to the posterior tibial nerve when the center of pressure (COP) was either 1.6 standard deviations anterior (COP(ant)) or posterior (COP(post)) to the mean baseline COP signal. Peak-to-peak amplitudes of the H-reflex and M-wave from the soleus (SOL) and medial gastrocnemius (MG) muscles were recorded to assess the efficacy of the Ia pathway. A significant increase in the H(max) : M(max) ratio for both the SOL (12 +/- 6%) and MG (23 +/- 6%) was observed during the COP(ant) as compared to the COP(post) condition. The source of the modulation between COP conditions cannot be determined from this study. However, the observed changes in the synaptic efficacy of the Ia pathway are unlikely to be simply a result of an altered level of background electromyographic activity in the triceps surae. This was indicated by the lack of differences observed in the H(max) : M(max) ratio when subjects stood without postural sway (via the use of a tilt table) at two levels of background activity. It is suggested that the phase-dependent modulation of the triceps surae H-reflexes during the postural sway of quiet standing functions to maintain upright stance and may explain the results from previous studies, which, until now, had not taken the influence of postural sway on the H-reflex into consideration.
  Acta Physiologica 12/2007; 191(3):229-36.
• Article: Reduced sarcoplasmic reticulum content of releasable Ca2+ in rat soleus muscle fibres after eccentric contractions.

  J S Nielsen, K Sahlin, N Ørtenblad
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  ABSTRACT: The purpose was to evaluate the effects of fatiguing eccentric contractions (EC) on calcium (Ca2+) handling properties in mammalian type I muscles. We hypothesized that EC reduces both endogenous sarcoplasmic reticulum (SR) content of releasable Ca2+ (eSRCa2+) and myofibrillar Ca2+ sensitivity. Isolated rat soleus muscles performed 30 EC bouts. Single fibres were isolated from the muscle and after mechanical removal of sarcolemma used to measure eSRCa2+, rate of SR Ca2+ loading and myofibrillar Ca2+ sensitivity. Following EC maximal force in whole muscle was reduced by 30% and 16/100 Hz force ratio by 33%. The eSRCa2+ in fibres from non-stimulated muscles was 45 +/- 5% of the maximal loading capacity. After EC, eSRCa2+ per fibre CSA decreased by 38% (P = 0.05), and the maximal capacity of SR Ca2+ loading was depressed by 32%. There were no effects of EC on either myofibrillar Ca2+ sensitivity, maximal Ca2+ activated force per cross-sectional area and rate of SR Ca2+ loading, or in SR vesicle Ca2+ uptake and release. We conclude that EC reduces endogenous SR content of releasable Ca2+ but that myofibrillar Ca2+ sensitivity and SR vesicle Ca2+ kinetics remain unchanged. The present data suggest that the long-lasting fatigue induced by EC, which was more pronounced at low frequencies (low frequency fatigue), is caused by reduced Ca2+ release occurring secondary to reduced SR content of releasable Ca2+.
  Acta Physiologica 12/2007; 191(3):217-28.
• Article: Glomerular sieving of three neutral polysaccharides, polyethylene oxide and bikunin in rat. Effects of molecular size and conformation.

  D Asgeirsson, D Venturoli, E Fries, B Rippe, C Rippe
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  ABSTRACT: Polysaccharides and many other non-protein polymers generally have a more open, flexible and asymmetrical structure compared with globular proteins. For a given molecular weight (MW), the Stokes-Einstein radius (a(e)) of the following polymers increases in the order: Ficoll < dextran <or= pullulan < polyethylene oxide (PEO). We have tested the hypothesis that such an increase in 'molecular extension' will increase the molecule's glomerular permeability. Thus, we investigated the glomerular sieving coefficients (theta) of the mentioned polymers and of the negatively charged and extended protein bikunin. In anaesthetized Wistar rats, glomerular sieving curves were generated for each FITC-labelled polymer from their respective concentration in urine and plasma, determined by size exclusion chromatography. The theta for bikunin was measured using a tissue uptake technique. For a molecule of a(e) = 55 A (cf. IgG), theta increased in the order: Ficoll (0.00035 +/- 0.000013) < dextran (0.022 +/- 0.0029) < pullulan (0.033 +/- 0.0024) < PEO (0.12 +/- 0.0055). For a(e) = 36 A (cf. albumin) the order was: Ficoll (0.076 +/- 0.0061) < dextran (0.45 +/- 0.037) = pullulan (0.45 +/- 0.021) < PEO (0.65 +/- 0.0076). theta for bikunin (0.089 +/- 0.0045) was 150 times higher than that of albumin, having an equivalent a(e) and net negative charge. From these results it is concluded that for flexible and asymmetric macromolecules, their degree of glomerular hyperpermeability is proportional to their degree of 'molecular extension'. Thus, compared with globular proteins, the polysaccharides investigated, including Ficoll, were found to be hyperpermeable across the glomerular filter in vivo.
  Acta Physiologica 11/2007; 191(3):237-46.
• Article: Intracellular signalling pathways in the vasoconstrictor response of mouse afferent arterioles to adenosine.

  P B Hansen, U G Friis, T R Uhrenholt, J Briggs, J Schnermann
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  ABSTRACT: Adenosine causes vasoconstriction of afferent arterioles of the mouse kidney through activation of adenosine A(1) receptors and Gi-mediated stimulation of phospholipase C. In the present study, we further explored the signalling pathways by which adenosine causes arteriolar vasoconstriction. Adenosine (10(-7) M) significantly increased the intracellular calcium concentration in mouse isolated afferent arterioles measured by fura-2 fluorescence. Pre-treatment with thapsigargin (2 microM) blocked the vasoconstrictor action of adenosine (10(-7) M) indicating that release of calcium from the sarcoplasmic reticulum (SR), stimulated presumably by IP(3), is involved in the adenosine contraction mechanism of the afferent arteriole. In agreement with this notion is the observation that 2 aminoethoxydiphenyl borate (100 microM) blocked the adenosine-induced constriction whereas the protein kinase C inhibitor calphostin C had no effect. The calcium-activated chloride channel inhibitor IAA-94 (30 microM) inhibited the adenosine-mediated constriction. Patch clamp experiments showed that adenosine treatment induced a depolarizing current in preglomerular smooth muscle cells which was abolished by IAA-94. Furthermore, the vasoconstriction caused by adenosine was significantly inhibited by 5 microM nifedipine (control 8.3 +/- 0.2 microM, ado 3.6 +/- 0.6 microM, ado + nifedipine 6.8 +/- 0.2 microM) suggesting involvement of voltage-dependent calcium channels. We conclude that adenosine mediates vasoconstriction of afferent arterioles through an increase in intracellular calcium concentration resulting from release of calcium from the SR followed by activation of Ca(2+)-activated chloride channels leading to depolarization and influx of calcium through voltage-dependent calcium channels.
  Acta Physiologica 11/2007; 191(2):89-97.
• Source

  Available from: PubMed Central

  Article: Molecular and functional expression of anion exchangers in cultured normal human nasal epithelial cells.

  J-H Shin, E J Son, H S Lee, S J Kim, K Kim, J Y Choi, M G Lee, J-H Yoon
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  ABSTRACT: Anions have an important role in the regulation of airway surface liquid (ASL) volume, viscosity and pH. However, functional localization and regulation of anion exchangers (AEs) have not been clearly described. The aim of this study was to investigate the regulation of AE mRNA expression level in accordance with mucociliary differentiation and the functional expression of AEs cultured normal human nasal epithelial (NHNE) cells. Nasal mucosal specimens from three patients are obtained and serially cultured cells are subjected to morphological examinations, RT-PCR, Western blot analysis and immunocytochemistry. AE activity is assessed by pHi measurements. Expression of ciliated cells on the apical membrane and expression of MUC5AC, a marker of mucous differentiation, increased with time. AE2 and SLC26A4 mRNA expression decreased as mucociliary differentiation progressed, and AE4, SLC26A7 and SLC26A8 mRNA expression increased on the 14th and 28th day after confluence. Accordingly, AE4 protein expression also progressively increased. AE activity in 100 mM K(+) buffer solutions was nearly twofold higher than that in 5 mM K(+) buffer solutions. Moreover, only luminal AE activity increased about fourfold over the control in the presence of 5 microM forskolin. In the presence of 100 microM adenosine-5'-triphosphate (ATP) which evokes intracellular calcium signalling through activation of purinergic receptors, only luminal AE activity was again significantly increased. On the other hand, 500 microM 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), an inhibitor of most SLC4 and SLC26AE isoforms, nearly abolished AE activity in both luminal and basolateral membranes. We found that AE activity was affected by intracellular cAMP and calcium signalling in the luminal membrane and was DIDS-sensitive in both membranes of cultured NHNE cells. Our findings through molecular and functional studies using cultured NHNE cells suggest that AEs may have an important role in the regulation of ASL.
  Acta Physiologica 11/2007; 191(2):99-110.
• Article: Aminoguanidine produces beneficial haemodynamic effects in a canine model of acute pulmonary thromboembolism.

  C A C Dias-Junior, J T C Sertorio, J E Tanus-Santos
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  ABSTRACT: Activating the nitric oxide (NO)-cyclic guanosine 3',5'-monophosphate (cGMP) pathway improves haemodynamics following acute pulmonary thromboembolism (APT). However, the role of NO synthase (NOS) isoforms in the responses to APT has not been determined. We examined the effects of selective and non-selective inducible NOS (iNOS) inhibition. Haemodynamic evaluations were performed in non-embolized dogs treated with saline (control group; n = 4), L-NAME (NAME group; n = 3), or aminoguanidine (AG group; n = 3), and in dogs that received the same drugs and were embolized with 5 mL kg(-1) of clots made with autologous blood (Emb group, n = 9; NAME + Emb group, n = 4 and AG + Emb group, n = 7). The lung concentrations of nitrite/nitrate (NOx) and cGMP were determined by chemiluminescence and ELISA respectively. Acute pulmonary thromboembolism increased mean pulmonary arterial pressure (MPAP) and pulmonary vascular resistance index (PVRI) by 21.4 +/- 1.7 mmHg and by 843 +/- 34 dyn s cm(-5) m(-2), respectively, in Emb group. MPAP and PVRI increased to higher levels in the NAME + Emb group 15 min after APT and all dogs in this group died 15-30 min after APT. Conversely, lower MPAP and PVRI levels were found in the AG + Emb group 2 h after APT compared with the Emb group (both P < 0.05). Higher NOx concentrations were found in the Emb group compared with the other groups (all P < 0.05). Higher cGMP concentrations were found in the Emb and AG + Emb groups compared with the other groups (all P < 0.05). These results indicate that endogenous NO protects against APT-induced cardiovascular responses. Moreover, iNOS-derived NO possibly produces unfavourable effects, which are counteracted by aminoguanidine. However, non-NO-related mechanisms may also be involved.
  Acta Physiologica 11/2007; 191(3):189-96.
• Article: Acute resistance exercise increases skeletal muscle angiogenic growth factor expression.

  T P Gavin, J L Drew, C J Kubik, W E Pofahl, R C Hickner
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  ABSTRACT: Both aerobic and resistance exercise training promote skeletal muscle angiogenesis. Acute aerobic exercise increases several pro-angiogenic pathways, the best characterized being increases in vascular endothelial growth factor (VEGF). We hypothesized that acute resistance exercise also increases skeletal muscle angiogenic growth factor [VEGF and angiopoietin (Ang)] expression. Seven young, sedentary individuals had vastus lateralis muscle biopsies and blood drawn prior to and at 0, 2 and 4 h post-resistance exercise for the measurement of VEGF; VEGF receptor [KDR, Flt-1 and neuropilin 1 (Nrp1)]; Ang1 and Ang2; and the angiopoietin receptor--Tie2 expression. Resistance exercise consisted of progressive knee extensor (KE) exercise to determine one repetition maximum (1-RM) followed by three sets of 10 repetitions (3 x 10) of KE exercise at 60-80% of 1-RM. Resistance exercise significantly increased skeletal muscle VEGF mRNA and protein and plasma VEGF protein at 2 and 4 h. Resistance exercise increased KDR mRNA and Tie2 mRNA at 4 h and Nrp1 mRNA at 2 and 4 h. Skeletal muscle Flt-1, Ang1, Ang2 and Ang2/Ang1 ratio mRNA were not altered by resistance exercise. These findings suggest that acute resistance exercise increases skeletal muscle VEGF, VEGF receptor and angiopoietin receptor expression. The increases in muscle angiogenic growth factor expression in response to acute resistance exercise are similar in timing and magnitude with responses to acute aerobic exercise and are consistent with resistance exercise promoting muscle angiogenesis.
  Acta Physiologica 11/2007; 191(2):139-46.