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  • American Physiological Society  (2)
  • 1
    Online Resource
    Online Resource
    ERK and p38 MAP kinase are involved in arachidonic acid release induced by H 2 O 2 and PDGF in mesangial cells
    American Physiological Society ; 2002
    In:  American Journal of Physiology-Renal Physiology Vol. 282, No. 3 ( 2002-03-01), p. F485-F491
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 282, No. 3 ( 2002-03-01), p. F485-F491
    Abstract: Increased prostaglandin production is implicated in the pathogenesis of glomerular disease. With this consideration, we examined the combined effects of reactive oxygen species and platelet-derived growth factor (PDGF), which might initiate glomerular dysfunction, on arachidonic acid release and cytosolic phospholipase A 2 (cPLA 2 ) activation in rat mesangial cells. H 2 O 2 -induced release of arachidonic acid was enhanced by PDGF, which by itself had little effect on the release, and the enhancement was completely inhibited by a cPLA 2 inhibitor. The phosphorylation of cPLA 2 , extracellular signal-regulated kinase (ERK), and p38 mitogen-activated protein (MAP) kinase was upregulated by H 2 O 2 or PDGF alone and except for ERK was enhanced further by the two in combination. The release of arachidonic acid induced by PDGF together with H 2 O 2 was inhibited partially by an inhibitor of ERK or p38 MAP kinase and completely when the two inhibitors were combined; the inhibitory pattern was similar to that for the phosphorylation of cPLA 2 . These results suggest that the ERK and p38 MAP kinase pathways are involved in the increase in cPLA 2 activation and arachidonic acid release induced by PDGF together with H 2 O 2 .
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.00210.2001
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2002
    detail.hit.zdb_id: 1477287-5
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  • 2
    Online Resource
    Online Resource
    Contribution of afferent pathway to vagal nerve stimulation-induced myocardial interstitial acetylcholine release in rats
    American Physiological Society ; 2020
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 319, No. 5 ( 2020-11-01), p. R517-R525
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 319, No. 5 ( 2020-11-01), p. R517-R525
    Abstract: Vagal nerve stimulation (VNS) has been explored as a potential therapy for chronic heart failure. The contribution of the afferent pathway to myocardial interstitial acetylcholine (ACh) release during VNS has yet to be clarified. In seven anesthetized Wistar-Kyoto rats, we implanted microdialysis probes in the left ventricular free wall and measured the myocardial interstitial ACh release during right VNS with the following combinations of stimulation frequency (F in Hz) and voltage readout (V in volts): F0V0 (no stimulation), F5V3, F20V3, F5V10, and F20V10. F5V3 did not affect the ACh level. F20V3, F5V10, and F20V10 increased the ACh level to 2.83 ± 0.47 ( P 〈 0.01), 4.31 ± 1.09 ( P 〈 0.001), and 4.33 ± 0.82 ( P 〈 0.001) nM, respectively, compared with F0V0 (1.76 ± 0.22 nM). After right vagal afferent transection (rVAX), F20V3 and F20V10 increased the ACh level to 2.90 ± 0.53 ( P 〈 0.001) and 3.48 ± 0.63 ( P 〈 0.001) nM, respectively, compared with F0V0 (1.61 ± 0.19 nM), but F5V10 did not (2.11 ± 0.24 nM). The ratio of the ACh levels after rVAX relative to before was significantly 〈 100% in F5V10 (59.4 ± 8.7%) but not in F20V3 (102.0 ± 8.7%). These results suggest that high-frequency and low-voltage stimulation (F20V3) evoked the ACh release mainly via direct activation of the vagal efferent pathway. By contrast, low-frequency and high-voltage stimulation (F5V10) evoked the ACh release in a manner dependent on the vagal afferent pathway.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.00080.2020
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2020
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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