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Träfflista för sökning "AMNE:(MEDICAL AND HEALTH SCIENCES Basic Medicine Physiology) ;pers:(Hellstrand Per)"

Sökning: AMNE:(MEDICAL AND HEALTH SCIENCES Basic Medicine Physiology) > Hellstrand Per

  • Resultat 1-10 av 81
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1.
  • Gomez-Pinilla, Pedro J, et al. (författare)
  • Melatonin restores impaired contractility in aged guinea pig urinary bladder
  • 2008
  • Ingår i: Journal of Pineal Research. - : Blackwell Publishing Ltd. - 1600-079X .- 0742-3098. ; 44:4, s. 416-425
  • Tidskriftsartikel (refereegranskat)abstract
    • Urinary bladder disturbances are frequent in the elderly population but the responsible mechanisms are poorly understood. This study evaluates the effects of aging on detrusor myogenic contractile responses and the impact of melatonin treatment. The contractility of bladder strips from adult, aged and melatonin-treated guinea pigs was evaluated by isometric tension recordings. Cytoplasmatic calcium concentration ([Ca2+](i)) was estimated by epifluorescence microscopy of fura-2-loaded isolated detrusor smooth muscle cells, and the levels of protein expression and phosphorylation were quantitated by Western blotting. Aging impairs the contractile response of detrusor strips to cholinergic and purinergic agonists and to membrane depolarization. The impaired contractility correlates with increased [Ca2+](i) in response to the stimuli, suggesting a reduced Ca(2+)sensitivity. Indeed, the agonist-induced contractions in adult strips were sensitive to blockade with Y27362, an inhibitor of Rho kinase (ROCK) and GF109203X, an inhibitor of protein kinase C (PKC), but these inhibitors had negligible effects in aged strips. The reduced Ca2+ sensitivity in aged tissues correlated with lower levels of RhoA, ROCK, PKC and the two effectors CPI-17 and MYPT1, and with the absence of CPI-17 and MYPT1 phosphorylation in response to agonists. Interestingly, melatonin treatment restored impaired contractility via normalization of Ca2+ handling and Ca2+ sensitizations pathways. Moreover, the indoleamine restored age-induced changes in oxidative stress and mitochondrial polarity. These results suggest that melatonin might be a novel therapeutic tool to palliate aging-related urinary bladder contractile impairment.
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2.
  • Lindqvist, Anders, et al. (författare)
  • Long-term effects of Ca(2+) on structure and contractility of vascular smooth muscle
  • 1999
  • Ingår i: American Journal of Physiology: Cell Physiology. - 1522-1563. ; 277:1, s. 64-73
  • Tidskriftsartikel (refereegranskat)abstract
    • Culture of dispersed smooth muscle cells is known to cause rapid modulation from the contractile to the synthetic cellular phenotype. However, organ culture of smooth muscle tissue, with maintained extracellular matrix and cell-cell contacts, may facilitate maintenance of the contractile phenotype. To test the influence of culture conditions, structural, functional, and biochemical properties of rat tail arterial rings were investigated after culture. Rings were cultured for 4 days in the absence and presence of 10% FCS and then mounted for physiological experiments. Intracellular Ca(2+) concentration ([Ca(2+)](i)) after stimulation with norepinephrine was similar in rings cultured with and without FCS, whereas force development after FCS was decreased by >50%. The difference persisted after permeabilization with beta-escin. These effects were associated with the presence of vasoconstrictors in FCS and were dissociated from its growth-stimulatory action. FCS treatment increased lactate production but did not affect ATP, ADP, or AMP contents. The contents of actin and myosin were decreased by culture but similar for all culture conditions. There was no effect of FCS on calponin contents or myosin SM1/SM2 isoform composition, nor was there any appearance of nonmuscle myosin. FCS-stimulated rings showed evidence of cell degeneration not found after culture without FCS or with FCS + verapamil (1 microM) to lower [Ca(2+)](i). The decreased force-generating ability after culture with FCS is thus associated with increased [Ca(2+)](i) during culture and not primarily caused by growth-associated modulation of cells from the contractile to the synthetic phenotype.
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3.
  • Albinsson, Sebastian, et al. (författare)
  • Arterial remodeling and plasma volume expansion in caveolin-1 deficient mice.
  • 2007
  • Ingår i: American Journal of Physiology: Regulatory, Integrative and Comparative Physiology. - : American Physiological Society. - 0363-6119 .- 1522-1490. ; 293, s. 1222-1231
  • Tidskriftsartikel (refereegranskat)abstract
    • Caveolin- 1 ( Cav- 1) is essential for the morphology of membrane caveolae and exerts a negative influence on a number of signaling systems, including nitric oxide ( NO) production and activity of the MAP kinase cascade. In the vascular system, ablation of caveolin- 1 may thus be expected to cause arterial dilatation and increased vessel wall mass ( remodeling). This was tested in Cav- 1 knockout ( KO) mice by a detailed morphometric and functional analysis of mesenteric resistance arteries, shown to lack caveolae. Quantitative morphometry revealed increased media thickness and media- to- lumen ratio in KO. Pressure- induced myogenic tone and flow- induced dilatation were decreased in KO arteries, but both were increased toward wild- type ( WT) levels following NO synthase ( NOS) inhibition. Isometric force recordings following NOS inhibition showed rightward shifts of passive and active length- force relationships in KO, and the force response to alpha 1- adrenergic stimulation was increased. In contrast, media thickness and force response of the aorta were unaltered in KO vs. WT, whereas lumen diameter was increased. Mean arterial blood pressure during isoflurane anesthesia was not different in KO vs. WT, but greater fluctuation in blood pressure over time was noted. Following NOS inhibition, fluctuations disappeared and pressure increased twice as much in KO ( 38 +/- 6%) compared with WT ( 17 +/- 3%). Tracer- dilution experiments showed increased plasma volume in KO. We conclude that NO affects blood pressure more in Cav- 1 KO than in WT mice and that restructuring of resistance vessels and an increased responsiveness to adrenergic stimulation compensate for a decreased tone in Cav- 1 KO mice.
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4.
  • Turczynska, Karolina, et al. (författare)
  • Regulation of vascular smooth muscle mechanotransduction by microRNAs and L-type calcium channels.
  • 2013
  • Ingår i: Communicative & Integrative Biology. - : Informa UK Limited. - 1942-0889. ; 6:1, s. 22278-22278
  • Tidskriftsartikel (refereegranskat)abstract
    • The phenotype of smooth muscle cells is regulated by multiple environmental factors including mechanical forces. Mechanical stretch of mouse portal veins ex vivo has been shown to promote contractile differentiation by activation of the Rho-pathway, an effect that is dependent on the influx of calcium via L-type calcium channels. MicroRNAs have recently been demonstrated to play a significant role in the control of smooth muscle phenotype and in a recent report we investigated their role in vascular mechanosensing. By smooth muscle specific deletion of Dicer, we found that microRNAs are essential for smooth muscle differentiation in response to stretch by regulating CamKIIδ and L-type calcium channel expression. Furthermore, we suggest that loss of L-type calcium channels in Dicer KO is due to reduced expression of the smooth muscle-enriched microRNA, miR-145, which targets CamKIIδ. These results unveil a novel mechanism for miR-145 dependent regulation of smooth muscle phenotype.
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5.
  • Lindqvist, Anders, et al. (författare)
  • Effects of oxygen tension on energetics of cultured vascular smooth muscle.
  • 2002
  • Ingår i: American Journal of Physiology: Heart and Circulatory Physiology. - : American Physiological Society. - 1522-1539 .- 0363-6135. ; 283:1, s. 110-117
  • Tidskriftsartikel (refereegranskat)abstract
    • Chronic hypoxia is a clinically important condition known to cause vascular abnormalities. To investigate the cellular mechanisms involved, we kept rings of a rat tail artery for 4 days in hypoxic culture (HC) or normoxic culture (NC) (PO(2) = 14 vs. 110 mmHg) and then measured contractility, oxygen consumption (JO(2)), and lactate production (J(lac)) in oxygenated medium. Compared with fresh rings, basal ATP turnover (J(ATP)) was decreased in HC, but not in NC, with a shift from oxidative toward glycolytic metabolism. JO(2) during mitochondrial uncoupling was reduced by HC but not by NC. Glycogen stores were increased 40-fold by HC and fourfold by NC. Maximum tension in response to norepinephrine and the JO(2) versus tension relationship (JO(2) vs. high K(+) elicited force) were unaffected by either HC or NC. Force transients in response to caffeine were increased in HC, whereas intracellular Ca(2+) wave activity during adrenergic stimulation was decreased. Protein synthesis rate was reduced by HC. The results show that long-term hypoxia depresses basal energy turnover, impairs mitochondrial capacity, and alters Ca(2+) homeostasis, but does not affect contractile energetics. These alterations may form a basis for vascular damage by chronic hypoxia.
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6.
  • Turczynska, Karolina, et al. (författare)
  • Stretch-Sensitive Down-Regulation of the miR-144/451 Cluster in Vascular Smooth Muscle and Its Role in AMP-Activated Protein Kinase Signaling.
  • 2013
  • Ingår i: PLoS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 8:5
  • Tidskriftsartikel (refereegranskat)abstract
    • Vascular smooth muscle cells are constantly exposed to mechanical force by the blood pressure, which is thought to regulate smooth muscle growth, differentiation and contractile function. We have previously shown that the expression of microRNAs (miRNAs), small non-coding RNAs, is essential for regulation of smooth muscle phenotype including stretch-dependent contractile differentiation. In this study, we have investigated the effect of mechanical stretch on miRNA expression and the role of stretch-sensitive miRNAs for intracellular signaling in smooth muscle. MiRNA array analysis, comparing miRNA levels in stretched versus non-stretched portal veins, revealed a dramatic decrease in the miR-144/451 cluster level. Because this miRNA cluster is predicted to target AMPK pathway components, we next examined activation of this pathway. Diminished miR-144/451 expression was inversely correlated with increased phosphorylation of AMPKα at Thr172 in stretched portal vein. Similar to the effect of stretch, contractile differentiation could be induced in non-stretched portal veins by the AMPK activator, AICAR. Transfection with miR-144/451 mimics reduced the protein expression level of mediators in the AMPK pathway including MO25α, AMPK and ACC. This effect also decreased AICAR-induced activation of the AMPK signaling pathway. In conclusion, our results suggest that stretch-induced activation of AMPK in vascular smooth muscle is in part regulated by reduced levels of miR-144/451 and that this effect may play a role in promoting contractile differentiation of smooth muscle cells.
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7.
  • Arheden, Håkan, et al. (författare)
  • Dissociation between force and [Ca2+]i during extra systoles in guinea-pig ventricular muscle microinjected with fura-2
  • 1999
  • Ingår i: Acta Physiologica Scandinavica. - : Wiley. - 0001-6772. ; 165:1, s. 1-8
  • Tidskriftsartikel (refereegranskat)abstract
    • Thin trabeculae were dissected from the right ventricle of guinea-pig heart and stimulated to contract isometrically at 0.5 Hz (26 degrees C). Rapid and transient changes of force were obtained by inducing three extra systoles (ES1-3) at 450-ms intervals. The two regular contractions (P1-2) following (ES1-3) were potentiated. Fura-2 salt was microinjected into the preparation to monitor intracellular calcium ([Ca2+]i). Three distinct phases of [Ca2+]i were seen: (1) a rapid rising phase to about 200 nmol L(-1), (2) a slower rising phase to a peak at 400 nmol L(-1), and (3) a slow decline to about 50 nmol L(-1). During ES1, there was a discrepancy between force, which decreased, and peak [Ca2+]i, which increased to 600 nmol L(-1). It is likely that the increased [Ca2+]i during the extra systoles reflects increased sarcolemmal calcium inflow, causing post-extra-systolic potentiation. Ryanodine (1-2 microM) was added to inhibit the intracellular calcium release and thus reduce the intracellular [Ca2+]i gradients following excitation. Ryanodine inhibited phase 1 of [Ca2+]i and abolished post-extra-systolic potentiation. There was a close relationship between dF/dt and [Ca2+]i with ryanodine during control and ES1-3. It is likely that fura-2 reports a spatially averaged [Ca2+]i and that phase 1 of the signal therefore apparently underestimates activator calcium in the close vicinity of the contractile elements.
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8.
  • Arheden, Håkan, et al. (författare)
  • Force-velocity relation and rate of ATP hydrolysis in osmotically compressed skinned smooth muscle of the guinea pig
  • 1987
  • Ingår i: Journal of Muscle Research and Cell Motility. - 0142-4319. ; 8:2, s. 151-160
  • Tidskriftsartikel (refereegranskat)abstract
    • Chemically skinned guinea pig taenia coli fibre bundles showed a concentration-dependent decrease in width when incubated in media containing Dextran T500 (0-0.2 g ml-1). The maximal reduction in width, observed at 0.2 g ml-1 dextran, was 32%. The effect was reversible upon removal of dextran. Isometric force was slightly increased (about 10%) at the lowest dextran concentration (0.025 g ml-1) but decreased at higher concentrations (40% decrease at 0.2 g/ml-1). The energetic tension cost (ATP turnover/force) was decreased by about 40% after dextran addition. Force development and relaxation were markedly slower in 0.1 g ml-1 and absent in 0.2 g ml-1 dextran. In isotonic quick-release experiments 0.025 g ml-1 dextran did not influence maximal shortening velocity (Vmax) and relative stiffness, whereas 0.1 g ml-1 markedly increased stiffness and decreased Vmax to about 27%. Vanadate induced relaxation in the activated muscle (pCa 4.5) both in the absence and presence (0.1 g ml-1) of dextran and increased the rate of relaxation (pCa 9) at 0.1 g ml-1 dextran. The isometric rate of crossbridge turnover, as reflected by the energetic tension cost and the rate of relaxation, was decreased at all degrees of osmotic compression. Crossbridge turnover rate during shortening (Vmax) was unaffected at an osmotic compression of 12% (width) but was decreased at higher compression (32%).
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9.
  • Hellstrand, Per, et al. (författare)
  • Mechanical transients in smooth muscle
  • 1989
  • Ingår i: Progress in Clinical and Biological Research. - 0361-7742. ; 315, s. 347-357
  • Tidskriftsartikel (refereegranskat)
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  • Resultat 1-10 av 81

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