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  • American Physiological Society  (5)
  • 1995-1999  (5)
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  • American Physiological Society  (5)
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  • 1995-1999  (5)
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  • 1
    Online Resource
    Online Resource
    American Physiological Society ; 1998
    In:  American Journal of Physiology-Cell Physiology Vol. 275, No. 2 ( 1998-08-01), p. C367-C374
    In: American Journal of Physiology-Cell Physiology, American Physiological Society, Vol. 275, No. 2 ( 1998-08-01), p. C367-C374
    Abstract: Because of the lack of salivary gland cell lines suitable for Ussing chamber studies, a recently established rat parotid acinar cell line, Par-C10, was grown on permeable supports and evaluated for development of transcellular resistance, polarization, and changes in short-circuit current ( I sc ) in response to relevant receptor agonists. Par-C10 cultures reached confluence in 3–4 days and developed transcellular resistance values of ≥2,000 Ω ⋅ cm 2 . Morphological examination revealed that Par-C10 cells grew as polarized monolayers exhibiting tripartite junctional complexes and the acinar cell-specific characteristic of secretory canaliculi. Par-C10 I sc was increased in response to muscarinic cholinergic and α- and β-adrenergic agonists on the basolateral aspect of the cultures and to ATP and UTP (through P2Y 2 nucleotide receptors) applied apically. Ion replacement and inhibitor studies indicated that anion secretion was the primary factor in agonist-stimulated I sc . RT-PCR, which confirmed the presence of P2Y 2 nucleotide receptor mRNA in Par-C10 cells, also revealed the presence of mRNA for the cystic fibrosis transmembrane conductance regulator and ClC-2 Cl − channel proteins. These findings establish Par-C10 cells as the first cell line of salivary gland origin useful in transcellular ion secretion studies in Ussing chambers.
    Type of Medium: Online Resource
    ISSN: 0363-6143 , 1522-1563
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1998
    detail.hit.zdb_id: 1477334-X
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    American Physiological Society ; 1997
    In:  American Journal of Physiology-Lung Cellular and Molecular Physiology Vol. 273, No. 4 ( 1997-10-01), p. L775-L781
    In: American Journal of Physiology-Lung Cellular and Molecular Physiology, American Physiological Society, Vol. 273, No. 4 ( 1997-10-01), p. L775-L781
    Abstract: Muscarinic receptor stimulation increases Ca 2+ sensitivity, i.e., the amount of force produced at a constant submaximal cytosolic Ca 2+ concentration ([Ca 2+ ] i ), in permeabilized smooth muscle preparations. It is controversial whether this increase in Ca 2+ sensitivity is in part mediated by protein kinase C (PKC). With the use of a β-escin permeabilized canine tracheal smooth muscle (CTSM) preparation, the effect of four putative PKC inhibitors {calphostin C, chelerythrine chloride, a pseudosubstrate inhibitor for PKC [PKC peptide-(19—31)], and staurosporine} on Ca 2+ sensitization induced by acetylcholine (ACh) plus GTP was determined. Preincubation with each of the inhibitors did not affect subsequent Ca 2+ sensitization induced by muscarinic receptor stimulation in the presence of a constant submaximal [Ca 2+ ] i , neither did any of these compounds reverse the increase in Ca 2+ sensitivity induced by ACh plus GTP. Administration of a 1,2-diacylglycerol analog, 1-oleoyl-2-acetyl- sn-glycerol, did not induce Ca 2+ sensitization at a constant submaximal [Ca 2+ ] i . Thus we found no evidence that PKC mediates increases in Ca 2+ sensitivity produced by muscarinic receptor stimulation in permeabilized CTSM.
    Type of Medium: Online Resource
    ISSN: 1040-0605 , 1522-1504
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1997
    detail.hit.zdb_id: 1477300-4
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    American Physiological Society ; 1999
    In:  American Journal of Physiology-Lung Cellular and Molecular Physiology Vol. 277, No. 2 ( 1999-08-01), p. L334-L342
    In: American Journal of Physiology-Lung Cellular and Molecular Physiology, American Physiological Society, Vol. 277, No. 2 ( 1999-08-01), p. L334-L342
    Abstract: This study determined whether the time-dependent decline in the rate of ATP hydrolysis by actomyosin ATPase during sustained isometric force can occur in the absence of a time-dependent decline in regulatory myosin light chain (rMLC) phosphorylation in Triton X-100-permeabilized canine tracheal smooth muscle. Maximal activation with 10 μM Ca 2+ induced sustained increases in isometric force, stiffness, and rMLC phosphorylation; however, the increase in the ATP hydrolysis rate was initially high but then declined to a steady-state level above that of the unstimulated muscle (basal 31.8 ± 5.8 nmol ⋅ cm −3 ⋅ s −1 ; peak 81.4 ± 11.3 nmol ⋅ cm −3 ⋅ s −1 ; steady-state 62.2 ± 9.1 nmol ⋅ cm −3 ⋅ s −1 ). Activation of strips in which the rMLC was irreversibly and maximally thiophosphorylated with adenosine 5′- O-(3-thiotriphosphate) also induced sustained increases in isometric force and stiffness but a nonsustained increase in ATP hydrolysis rate. There was no significant difference in the peak or steady-state isometric force, stiffness, or ATP hydrolysis rate or in the steady-state maximum unloaded shortening velocity between strips activated by 10 μM Ca 2+ or rMLC thiophosphorylation (0.058 ± 0.016 and 0.047 ± 0.011 muscle lengths/s, respectively). Mechanisms other than changes in rMLC phosphorylation contribute to the time-dependent decline in actomyosin ATPase activity during sustained activation of canine tracheal smooth muscle.
    Type of Medium: Online Resource
    ISSN: 1040-0605 , 1522-1504
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1999
    detail.hit.zdb_id: 1477300-4
    SSG: 12
    Location Call Number Limitation Availability
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  • 4
    Online Resource
    Online Resource
    American Physiological Society ; 1998
    In:  Journal of Applied Physiology Vol. 84, No. 2 ( 1998-02-01), p. 754-758
    In: Journal of Applied Physiology, American Physiological Society, Vol. 84, No. 2 ( 1998-02-01), p. 754-758
    Abstract: Dyke, Christopher K., Niki M. Dietz, Robert L. Lennon, David O. Warner, and Michael J. Joyner. Forearm blood flow responses to handgripping after local neuromuscular blockade. J. Appl. Physiol. 84(2): 754–758, 1998.—To test the hypothesis that acetylcholine “spillover” from motor nerves contributes significantly to skeletal muscle vasodilation during exercise, we measured the forearm blood flow responses during attempted handgripping after local paralysis of the forearm with the neuromuscular-blocking drug pipecuronium. This compound blocks postsynaptic nicotinic receptors but has no impact on acetylcholine release from motor nerves. The drug was administered selectively to one forearm by using regional intravenous drug administration techniques in five subjects. Pipecuronium reduced maximum forearm grip strength from 40.0 ± 3.2 kg before treatment to 0.0 kg after treatment. By contrast, drug administration had no effect on maximum voluntary contraction in the untreated forearm (41.3 ± 3.3 vs. 41.4 ± 2.7 kg). During 2 min of attempted maximal contraction of the paralyzed forearm, the forearm blood flow increased from only 3.4 ± 0.8 to 4.8 ± 1.2 ml ⋅ 100 ml −1 ⋅ min −1 ( P 〈 0.05). Heart rate increased from 63 ± 3 to 73 ± 8 beats/min ( P 〉 0.05) during attempted contraction, and only three of five subjects showed obvious increases in heart rate. Mean arterial pressure increased significantly ( P 〈 0.05) from 102 ± 6 to 109 ± 9 mmHg during attempted contractions. When these increases in flow are considered in the context of the marked (10-fold or greater) increases in flow seen in contracting forearm skeletal muscle, it appears that acetylcholine spillover from motor nerves has, at most, a minimal impact on the hyperemic responses to contraction in humans.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1998
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 5
    Online Resource
    Online Resource
    American Physiological Society ; 1999
    In:  American Journal of Physiology-Lung Cellular and Molecular Physiology Vol. 277, No. 4 ( 1999-10-01), p. L816-L822
    In: American Journal of Physiology-Lung Cellular and Molecular Physiology, American Physiological Society, Vol. 277, No. 4 ( 1999-10-01), p. L816-L822
    Abstract: The purpose of this study was to determine the mechanism by which hydrogen peroxide (H 2 O 2 ), an important inflammatory mediator, relaxes canine tracheal smooth muscle (CTSM). H 2 O 2 caused concentration-dependent relaxations of CTSM strips contracted with ACh or isotonic KCl [EC 50 of 0.24 ± 0.04 (SE) and 0.23 ± 0.04 mM, respectively]. Indomethacin (10 μM) decreased the sensitivity of both KCl- and ACh-contracted strips to H 2 O 2 . H 2 O 2 increased intracellular cAMP levels, an increase that was abolished by indomethacin. H 2 O 2 did not affect intracellular cGMP levels. In strips treated with indomethacin and contracted with ACh or isotonic KCl, H 2 O 2 -evoked relaxations were accompanied by increases in intracellular Ca 2+ concentration and decreases in regulatory myosin light chain phosphorylation. We conclude that H 2 O 2 decreases Ca 2+ sensitivity in CTSM by decreasing regulatory myosin light chain phosphorylation through inhibition of myosin light chain kinase and/or activation of smooth muscle protein phosphatases.
    Type of Medium: Online Resource
    ISSN: 1040-0605 , 1522-1504
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1999
    detail.hit.zdb_id: 1477300-4
    SSG: 12
    Location Call Number Limitation Availability
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