Pharmacological Research, VU. 26, Supplement I, 1992
PRELIMINARY CRARACTERIZATION GLDCOCORTICOIDS IN ENDoTBEm
Teresa Iuvone, Department "Federico
of Rxperimental 11~~.
OF VASOCORTIN CELTS.
and Massimo Di Rosa
Vasocortin is a glucocorticoid-induced anti-inflammatory protein which inhibits dextran oedema and histamine release from rat mast cells (1). In the present study the induction of vasocortin in bovine and human endothelial cells as well as G M 7373 cell-line has been investigated. The biological activity of vasocortin recovered from the culture medium of bovine endothelial cells and G M 7373 cell-line was mainly associated with proteins having a m .w. in the range of 20-35 Kd. Partially purified vasocortin inhibited in a concentration related fashion histamine release induced in rat mast-cells by concanavalin A. In contrast vasocortin did not inhibit histamine release induced by either calcium ionophore A23187 or compound 48/80. These data suggest that endothelial cells may be a target of glucocorticoids in and show that vasocortin m imics vascular tissue the inhibitory effect of corticosteroids on histamine release. Carnuccio R., Di Rosa M ., Ialenti A., Iuvone 1. Sautebin L. Br. J. Pharmacol. 1989; 98: 32-34.
EXOGENOUSNITRIC OXIDE INDUCES ACUTE INFLAMMATION A. Ialenti, A. Ianaro, S. Moncada* and M . Di Rosa Dept. of Experimental Pharmacology, University of Naples * Wellcome Research Laboratories, Beckenham, Kent, U.K. We have previously shown that endogenous nitric oxide (NO) modulates acute inflammation (1). In this study we present direct evidence that exogenous NO increases vascular We have permeability and induces oedema formation. investigated the phlogogenic activity of the following NOthe active metabolite of molsidomine, SNP donors: SIN-l, SNAP (S-nitroso-N-acetylnitroprusside), (sodium were injected These compounds D,L,penicillamine). intradermally or into the paw of male Wistar rats. All NOdonors tested were able to induce both an increase in vascular permeability and oedema formation. These effects were dependent on NO release since they were inhibited by methylene blue and enhanced by SOD. These results are the first evidence that NO is able to induce an acute inflammatory response. (1) Ialenti A., Ianaro A., Moncada S. md Di Rosa M. (1992) Eur. J. Pharmacol., 211, 177-182