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Intraventricular injection of beta-endorphin (3, 7, 10 and 30 nmol/kg) into the third ventricular of pentobarbital-anaesthetized male Sprague-Dawley rats resulted in a dose-dependent increase in mean arterial pressure (MAP) while injection of the same volume of 0.9% NaCl solution did not cause significant changes in MAP. Naloxone, which did not produce any significant change in MAP, antagonized the vasopressor effect of beta-endorphin, indicating that the response is mediated via the naloxone sensitive opiate receptors. Rats acclimated to cold (5 degrees) for 3 weeks showed a potentiated and prolonged increase in MAP following beta-endorphin injection, indicating an increased responsiveness to the peptide. This increased responsiveness in the cardiovascular system is probably of adaptive value in cold acclimation. Naloxone itself did not alter MAP either, but abolished the cardiovascular response to beta-endorphin completely in cold acclimated rats, indicating an increased effectiveness in its antagonistic effect following cold acclimation as well. 相似文献
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Hubert M Tse Steven I Josephy Edward D Chan Darren Fouts Andrea M Cooper 《Journal of immunology (Baltimore, Md. : 1950)》2002,168(2):825-833
Of the two common morphotypes of Mycobacterium avium, designated smooth transparent (SmT) or smooth opaque (SmO), the SmO morphotype is avirulent, whereas the SmT morphotype is virulent. The role of the host macrophage in determining these different virulence phenotypes was analyzed using an in vitro model of macrophage infection. Initial studies confirmed previous reports of the increased ability of the SmT bacteria to grow in macrophages; this increased virulence correlated with reduced induction of inflammatory cytokines. Examination of the response of the mitogen-activated protein kinase (MAPK) pathway following infection with either morphotype revealed that all three members of the MAPK pathway were activated. Pharmacologic inhibition of either the extracellular signal-regulated kinase (ERK) or p38(MAPK) pathways resulted in distinct consequences for the growth of the two morphotypes. In particular, inhibition of the p38(MAPK) resulted in attenuated growth of the SmT morphotype, which correlated with reduced PGE(2) production. Inhibition of cyclooxygenase 2 by indomethacin also inhibited growth of SmT, substantiating the role for PGE(2) in promoting the growth of SmT. In contrast, SmO induction of the ERK pathway was increased compared with the SmT morphotype, and inhibition of ERK resulted in decreased TNF-alpha synthesis and enhanced SmO growth. Pharmacologic inhibitors of the MAPK pathway were present for only the first 4 h of infection and yet had consequences for bacterial growth at 7 days. Therefore, the data suggest that induction of the MAPK pathway during uptake of bacteria is instrumental in determining the eventual fate of the bacteria. 相似文献