Abstract
Exogenous catecholamines have been proved to be active in the reduction of vascular permeability induced by various inflammatory mediators viaβ-adrenoceptor activation, but it is not known whether an endogenousβ-adrenergic agonist has any effect. We studied it in skin and lung vessels. The results revealed that an intravenous bolus of isoproterenol (10μg/kg) attenuated platelet-activating factor-and histamine-induced Evans blue dye extravasation in rat dorsal skin, while intraperitoneal administration ofβ-adrenoceptor blocker propranolol (0.1 mg/kg) significantly increased the dye extravasation. Blockade ofβ-adrenoceptor by propranolol for 12 h noticeably increased wet/dry lung weight ratio, lung water content, bronchoalveolar lavage (BAL) protein concentration, leukocyte count, and lipoperoxide degradation product malondialdehyde (MDA) content. In isolated perfused lung in vitro, propranolol (2.5μg/ml) had no obvious effects on lung weight gain, fluid filtration coefficient, and pulmonary vascular pressure during the 20-min perfusion compared with control. The results suggested that endogenousβ-adrenergic agonist is an important factor in the maintenance of vascular integrity and the quiescent state of leukocytes, indicating the antiinflammatory role of catecholamines in physiological states and critical illnesses.
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References
Inagaki, N., T. Miura, H. Nagai, andH. Koda. 1992. Antiallergic mechanisms of betaadrenergic stimulants in rats.Life Sci. 51:PL201-PL205.
Boxer, L. A., J. M. Allen, andR. L. Baehner. 1980. Diminished polymorphonuclear leukocyte adherence. Function dependent on release of cyclic AMP by endothelial cells after stimulation ofβ-receptors by epinephrine.J. Clin. Invest. 66:268–274.
Minnear, F. L., M. A. A. Demichele, D. G. Moon, C. L. Rieder, andJ. W. Fenton II. 1989. Isoproterenol reduces thrombin-induced pulmonary endothelial permeability in vitro.Am. J. Physiol. 257:H1613-H1623.
Fonteh, A. N., J. D. Winkler, T. J. Torphy, J. Heravi, B. J. Undem, andF. H. Chilton. 1993. Influence of isoproterenol and phosphodiesterase inhibitors on platelet-activating factor biosynthesis in the human neutrophil.J. Immunol. 151:339–350.
Ding, Z. Q., S. H.Li, M. Z.Jiang, and Z. L.Wu. 1994. Suppression by isoproterenol of endothelial cell morphology and barrier function changes induced by platelet-activating factor.Inflammation (in press).
Ding, Z. Q., S. H. Li, andZ. L. Wu. 1992. Mechanisms of endothelial cell-dependent leukocyte adhesion stimulated by platelet-activating factor.Inflammation 16:179–186.
Allison, R. C., E. M. Hernandez, V. R. Prasad, M. B. Grisham, andA. E. Taylor. 1988. Protective effects of O2 radicle scavengers and adenosine in PMA-induced lung injury.J. Appl. Physiol. 64:2175–2182.
Majno, G., V. Gilmore, andM. Leventhal. 1967. On the mechanism of vascular leakage caused by histamine-type mediators. A microscopic study in vivo.Circ. Res. 21:833–847.
Curry, F. E. 1992. Modulation of venular microvessel permeability by calcium influx into endothelial cells.FASEB J. 6:2456–2466.
Grega, G. J. 1986. Contractile elements in endothelial cells as potential targets for drug action.Trends Pharmacol. Sci. 7:452–456.
Warren, J. B. 1993. Vascular control of inflammatory edema.Clin. Sci. 84:581–584.
Wysolmerski, R. B., andD. Lagunoff. 1990. Involvement of myosin light-chain kinase in endothelial cell retraction.Proc. Natl. Acad. Sci. U.S.A. 87:16–20.
Langeler, E. G., andV. W. M. Van Hinsbergh. 1991. Norepinephrine and iloprost improve barrier function of human endothelial cell monolayers: Role of cAMP.Am. J. Physiol. 260:C1052-C1059.
Stelzner, T. J., J. V. Weil, andR. F. O'Brien. 1989. Role of cyclic adenosine monophosphate in the induction of endothelial barrier properties.J. Cell. Physiol. 139:157–166.
Minnear, F. L., A. Johnson, andA. B. Malik. 1986.β-adrenergic modulation of pulmonary transvascular fluid and protein exchange.J. Appl. Physiol. 60:266–274.
Seibert, A. F., W. J. Thompson, A. Taylor, W. H. Wilborn, J. Barnard, andJ. Haynes. 1992. Reversal of increased microvascular permeability associated with ischemia-reperfusion: Role of cAMP.J. Appl. Physiol. 72:389–395.
Siflinger-Birnboim, A., D. C. Bode, andA. B. Malik. 1993. Adenosine 3′, 5′-cyclic monophosphate attenuates neutrophil-mediated increase in endothelial permeability.Am. J. Physiol. 264:H370-H375.
Mizus, I., W. Summer, I. Farrukh, J. R. Michael, andG. H. Gurtner. 1985. Isoproterenol or aminophylline attenuate pulmonary edema after acid lung injury.Am. Rev. Respir. Dis. 131:256–259.
Killackey, J. J. F., M. G. Johnston, andH. Z. Movat. 1986. Increased permeability of microcarrier-cultured endothelial monolayers in response to histamine and thrombin. A model for the in vitro study of increased vasopermeability.Am. J. Pathol. 122:50–61.
Bottaro, D., D. Shepro, S. Peterson, andH. B. Hechtman. 1986. Serotonin, norepinephrine, and histamine mediation of endothelial cell barrier function in vitro.J. Cell. Physiol. 128:189–194.
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Grant support: National Natural Science Foundation of China 39200144.
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Ding, Z., Jiang, M., Li, S. et al. Vascular barrier-enhancing effect of an endogenousβ-adrenergic agonist. Inflammation 19, 1–8 (1995). https://doi.org/10.1007/BF01534375
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DOI: https://doi.org/10.1007/BF01534375